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Appendix: Tricky Topic Transcripts

Tricky Topic Transcripts

In order of appearance:

1031 Tricky Topics

Tricky Topic: Introduction to Research Design

Slide 1: Research Design (Introduction)
Research is the foundation of science, as such, understanding research design is essential for basic science literacy. Let’s begin by discussing some of the basic components of research.

Slide 2: Basics
The first term you should be comfortable with is, “variable”. Simply put, a variable is any factor that varies within a specified group or population; some examples are height, weight, caffeine intake, and blood pressure. So, if we’re interested in whether caffeine affects blood pressure, we might research this by measuring the variables: 1) daily caffeine intake and 2) blood pressure.
The second term that’s important is population.
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In research design this refers to the entire group that we’re interested in knowing more about. For example if we’re interested in knowing whether sugar makes kids hyperactive, the group or population we’re interested in are all children. If we’re interested in Alzheimer’s disease then the population would be all people with Alzheimer’s disease. You can see that the population is dependent on the research question. As you can imagine, a population can be very large, for instance there are a LOT of children in the world, making it impossible to test them all, so to make things more manageable we can instead take a sample
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or subset of the population of interest. The important thing is to make sure that the sample is REPRESENTATIVE of the population,
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meaning that the sample has the same overall makeup as the larger population. You wouldn’t want to ask a question about children and then only test females, because the population of children, of course, is made up of more than just girls. If we want results that are applicable to the population we’re interested in, then we need our sample to match that population.
Okay, Now that we have some of the basics under our belt, we can move on to specific types of research designs.

Slide 3: Types of Research Designs
In general we can divide research designs into three different categories. The first category is what’s known as descriptive research.
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Descriptive research, as the name implies, involves describing phenomena like: how many hours of TV do most people watch per day, or what types of behaviours do children engage in on the playground, or what types of study habits do university students employ. These are all examples of questions that can be addressed with descriptive research.
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The next type of research design is what’s known as correlational research. Correlational research involves looking at the relationships between variables
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for instance, how is X related to Y? When X goes up does Y also go up? Or when X goes up does Y go down?
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The third type of research design is what’s known as an experimental design. Experimental design is considered the gold standard in the research world as it involves not just the measurement, but also the MANIPULATION of specific variables.
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This type of design allows us to make the strongest conclusions. In an experimental design what we’re asking is whether or not something causes something else. For instance, does my new drug cause a decrease in depression like symptoms.

Slide 4: Research Design (Introduction)
That concludes our introductory look at the three types of research design: descriptive research; correlational research; and experimental research.

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Tricky Topic: Descriptive Research Design

Slide 1: Research Design (Descriptive Design)
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Slide 2: Types of Research Designs
Let’s focus in on the first of the three research design types: descriptive design.

Slide 3: Types of Descriptive Designs
Descriptive designs can be further grouped into three different types.
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The first of the three types is a case study. In a case study, researchers carefully observe or describe behaviour in a single individual, or in some cases, a very small group. This type of design tends to be used when focusing on a unique case like a rare disease, or an event, that only a small number of people experience. Based on the information collected from a case study, we cannot make any broad conclusions, however, information gathered from a case study can help us increase our understanding of unusual behaviours, which may be impossible to study otherwise.
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The second type of descriptive design is naturalistic observation. Naturalistic observation is observing an individual in their natural environment. For example, famous primatologist, Jane Goodall, used this method to first document tool use in chimpanzees.
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Although this method is most often used to describe animal behaviour, it can also been used to study human behaviour.
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For example, Canadian researchers Debra Pepler and Wendy Craig have used naturalistic observation to provide a rich description of bullying behaviours in school playgrounds.
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The third type of descriptive design involves interviews and surveys. Interviews and surveys can be done in person or via phone or online. Importantly, they can allow researchers to collect vast amounts of information from many individuals, so they can be quite useful.

Slide 4: Research Design (Descriptive Design)
Taken together, descriptive research can be an excellent starting point – it allows us to better understand what’s happening. However, because we are only describing what we are observing we cannot be sure what is actually causing an observed phenomenon to occur. For this reason, descriptive research is typically used to get the lay of the land before moving on to more complex research designs.

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Tricky Topic: Correlational Research Design

Slide 1: Research Design (Correlational Design)
Correlational designs take descriptive research one step further.

Slide 2: Types of Research Designs
Correlational designs seek to understand how variables are related to one another.

Slide 3: Correlational Designs
This relationship between variables is often expressed as a correlation coefficient. A correlation coefficient is a number that ranges between positive 1 and negative 1. The number itself represents the strength of the relationship between two variables. So, as an example, a correlation coefficient of 0.8 would be a strong relationship whereas a correlation coefficient of 0.2 would be much weaker. The positive or negative of the correlation coefficient tells us the direction of the relationship: if it’s positive, it means that as the value of one variable increases or decreases, then the second variable also increases or decreases in the same manner. If the correlation coefficient is a negative number, then as the value of one variable increases the other decreases (and vice versa). This is best illustrated with some examples.
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This figure shows a type of graph called a SCATTERPLOT. Each data point on the graph represents two variables for a single person. On the horizontal axis, also called the x-axis, we have height, and on the vertical axis, also called the y-axis, we have shoe size. By looking at the data points on this figure we can see as peoples height increases, so does their shoe size. Thus, the data points on this scatterplot show a positive relationship,
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because the values increase together in the same direction with a correlation coefficient of +0.93, which is a strong positive correlation since it’s quite close to +1. This is not surprising since taller people tend to have larger feet than smaller people.
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This scatterplot is similar to the last one as the vertical y-axis shows shoe size. However, notice that the horizontal x-axis is now different. The x-axis now shows a person’s final grade in a course. The data points are scattered all over the place,
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which tells us, not surprisingly, that there is no relationship between shoe size and final exam score, the correlation coefficient is pretty close to 0.
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Finally, This last scatterplot shows final grades on the x-axis, and hours per day of watching Netflix on the y-axis. The data shows a clear negative relationship,
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so the more time spent watching Netflix, the LOWER the final grade in the course; this correlation coefficient is pretty close to -1.
As demonstrated, correlational designs can tell us a lot about the relationship between two variables and so are very useful and are frequently used in psychology. Let’s focus in now on another example to help us see why psychologists might choose to address their research questions with a correlational design.

Slide 4: Using Correlational Designs
Imagine you are interested in whether the amount of screen time increases short-sightedness in children. Do you think as a researcher you would be able to take away all laptops and televisions from some children while imposing certain durations of screen time on others? Most definitely not! It’s neither practical nor ethical to carry out this type of study. However, what you could do is look at whether a child is short-sighted or not as well as the average amount of time they spend looking at a screen. So, in this way you would be looking at the relationship between screen time and short-sightedness without depriving or enforcing technology on children. For these reasons, correlational designs are often necessary and as a result are frequently used. Of course, it is also for these reasons that correlational designs come with limitations.

Slide 5: Limitations of Correlations
The biggest limitation of correlational designs is that they cannot determine causality. One reason for this is the directionality problem, meaning it’s not possible to tell the direction of causation. For instance, let’s say there is a strong correlation between sitting close to the TV and poor vision.
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You might conclude that sitting close to the screen CAUSES poor vision. But, it’s also possible that poor vision leads people wanting to sit closer to the TV, so they can see. With a correlational design, we are not able to tell whether one variable causes the other, only that the variables are linked. Another reason why we can’t determine causality from correlation is the third variable problem,
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which presents the possibility that the cause could be something else entirely. What if actually, sitting too close to the television and poor vision are both being caused by a third variable that wasn’t measured, or in some case, not even realized. For our current example, a third variable could be the amount of time spent indoors.
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It might be that spending time inside leads to both people spending more time watching TV as well as poor vision. In fact, a recent study in China showed that time spent indoors was a predictor of needing glasses in children, not screen time! So, directionality and third variables must be taken into consideration when interpreting correlations between variables.

Slide 6: Research Design (Correlational Design)
While correlational designs can illuminate strong relationships between variables, they must always be interpreted with caution. As we discussed, causation can never be inferred from correlation. To determine causation, experimental research design is required.

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Tricky Topic: Experimental Research Design

Slide 1: Research Design (Experimental Design)
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Slide 2: Types of Research Designs
Unlike the other research designs, the experimental method allows for the manipulation of specific variables.

Slide 3: Experimental Design
Experimental design allows you to ask the question,
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does X cause Y? For example, does sugar cause hyperactivity in children? In an experiment, the researcher manipulates one or more variables, and measures others, while attempting to control for all other factors. By controlling the environment, it ensures that the only difference between the groups is a difference in the variable of interest. So, an experimental research design has two different types of variables,
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the independent variable, and dependent variable. The independent variable is the one that’s manipulated and is the proposed cause in the research question. If we go back to the example of whether sugar causes hyperactivity in children, this would be sugar. The dependent variable is the one that’s measured, and it’s the proposed effect in the research question, so back to our question of whether sugar causes hyperactivity in children, this would be activity levels. Although an experiment can have many independent and dependent variables, the most basic experimental design has to have at least one independent variable and one dependent variable. Let’s design a simple experiment to ask about the effect of sugar on the activity levels in children.

Slide 4: Designing an Experiment
In this experiment we’re interested in the effect of sugar, so we’re going to try to keep everything else the same. Then we can compare whether the group given sugar is more active than the group that did not receive sugar. If we design our experiment carefully, we can potentially conclude that a difference in activity is being caused by sugar or is not. So, first we recruit a sample of participants…
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In order to ensure that the groups are comparable before the we start the experimental manipulation, it’s best to RANDOMLY assign our participants to groups.
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The first group receives sugar whereas the second group receives a sweet substance without sugar, in this case we’ll use artificial sugar. The group that received the active ingredient, sugar, we call the experimental group,
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while the group that did not receive the active ingredient, but instead received artificial sugar, is known as the control group.
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At this point in our experimental design we’ve just manipulated our independent variable.
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Remember, our dependent variable measures the possible effect of the independent variable; it depends on the independent variable. So, in both of our two groups we are going to measure activity levels.
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This will allow us to see whether or not the sugar is causing a change in the activity level. Now, if we see a difference in the activity level by statistically comparing the two groups
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and notice that the activity levels for the children in the experimental group (those that received sugar) are higher than the children in the control group (those that did not receive sugar), we can conclude that the sugar caused this effect. This is because we have theoretically controlled all other possible variables leaving the only change between the groups of whether or not they received sugar. Further, if we don’t see a difference between the two groups then, we can conclude that the sugar did not contribute to an increase in activity.

Slide 5: Research Design (Experimental Design)
That concludes our look at experimental design. Unlike other types of designs, it is only with experimental designs that we can test causative relationships.

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Tricky Topic: Statistical Measures

Slide 1: Statistical Measures
It’s usually necessary to do some number crunching in order to make sense of data collected as part of a research study. Statistics is the field of mathematics involved with collecting, analyzing, presenting, and interpreting data.
In this Tricky Topic, you’ll become familiar with some commonly used statistical measures.

Slide 2: Statistics and Math
Math tends to be a polarizing topic – you either love it or hate it, kind of like olives or black liquorice. but it’s necessary to embrace your inner mathematician if you want to understand how research findings are represented statistically. To do that, let’s look at an example of some data you might be interested in, performance on a class quiz.

Slide 3: Quiz Performance Data
Let’s say we have 19 students in our class who have just finished a quiz, graded out of 10. Looking at this list of numbers isn’t the most efficient way to figure out how these students did overall. I mean we can see just with a quick scan that Mashoodh and Redden got the highest marks and Stamp got the lowest. If the class was much bigger than this, it would be really difficult and time-consuming to scan through the data by eye. One way to get a better sense of quiz performance is to arrange the grades from lowest to highest, rather than alphabetically.
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This gives us an even clearer picture of how the class did, for instance we can see that quite a few students got 7/10.

Slide 4: Displaying Frequency
Something else you can do is to display the data in a graph by plotting a frequency distribution. Basically you put your measure of interest on the x-axis on the bottom, in this case quiz scores, and the number of people who got each score on the y-axis on the left. Again, it’s obvious that most people got a 7,
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but we can see the overall pattern of grades more easily in this figure compared to the table. A frequency distribution is a great way to eyeball your data, but it’s not the only way. Researchers use a number of descriptive statistics to communicate findings in a data set.

Slide 5: Common Descriptive Statistics
Measures of central tendency produce a single value that is typical of the whole data set. These are handy because they relay information about the data without having to scan the whole collection. The most commonly reported measure of central tendency is the mean,
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which is the mathematical average, represented by the symbol x-bar. To calculate the mean, you have to add up or sum, shown by this symbol here,
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all of your values, which we affectionately refer to as x.
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Then we divide this sum by the number of observations we have in total, which in stats-speak is referred to as n.
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The median is another measure of central tendency that is the midpoint value in your data set,
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while the mode is the most frequently occurring value. Let’s look at these measures of central tendency in our quiz scores.

Slide 6: Measures of Central Tendency
By adding up all the numbers and dividing our n, the number of quizzes, our mean works out to 6.4.
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Note that not one of the students actually scored a 6.4, since it wasn’t a possible value, but it does give us a sense of how the group did as a whole. The median is 7,
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because if you arrange the values from smallest to largest, 7 is in the middle: there are 9 values less than 7, and 9 values more than 7. The mode is also 7,
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because it’s the most frequently occurring score, five students got a 7.
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This gives us a very similar idea to what we saw in the frequency distribution we saw earlier, which told us that the scores on this quiz centred around 7.

Slide 7: Common Descriptive Statistics
Other commonly used statistics are measures of variability, or spread of scores in a data set. The simplest measure of variability is the range,
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which is the span between the highest and lowest values.
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For our quiz, the highest score was a 9 and the lowest score was a 3, so the range is 6.
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The degree of spread in quiz performance can also be calculated in a similar way to how we determined the mean. One common measure is variance,
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represented as s2, a number that indicates how much the individual scores deviate from the mean, and is calculated using squares. Let me explain.
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Keep in mind that the mean for this quiz is 6.4 out of a possible max of 10. We can simply work out how much each value differs from the mean, so 3 minus 6.4 is -3.4, and 4 minus 6.4 equals -2.4, and so on. And then take the average deviation. Note that these data points give us negative values. After we’ve finished calculating each value’s deviation, if we add all of these together in order to find the average, we run into a problem: the positives and negatives cancel each other out, so you end up with a grand total close to zero.
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Well that doesn’t appear to tell us very much about the spread of data because it makes it seem like there’s no variability at all, and there clearly is – we saw what the data looked like, and we also calculated a range of 6. There’s a simple mathematical solution to this problem. What we can do is square the individual deviations.
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Like shown here, because a negative times a negative equals a positive, so that gives us a way to add these up. As long as we do the same thing to all of the values, this doesn’t break any math rules. We add up these numbers to get our total squared deviation.
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Here is the variance equation.
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It’s the sum of each observation (so each quiz) minus the mean, squared – to avoid numbers cancelling each other out – divided by n minus 1.
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Once we plug in our total deviation into our equation and divide by n minus 1, we get a mean squared deviation, or variance of 2.8. Values larger than this would indicate more spread in the values, and values less than this tell us that the scores are more closely clustered together. If you’re wondering why it’s n minus 1, don’t worry about that for our purposes. Some clever statistician calculated that n minus 1 is more accurate to predict variability than just dividing by n like we did for the mean. What you will see reported more often, however, is the standard deviation.
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This takes the square root of the variance, and the number we get is roughly 1.7,
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it’s in the same form as the scores that we used to get the mean. Keep in mind you don’t have to bother with squares or square roots to calculate the mean because the mean doesn’t give us a mix of positive and negative values. The standard deviation is used a lot for other types of statistical calculations, so it’s useful to know where it comes from. If you’re a math-head, then you might find this interesting, but if you’re math-phobic then you might be wondering when the heck you’ll ever need to know this. Well, one area of research in psychology where standard deviation plays a big part is intelligence testing. Wechsler’s IQ tests are the most widely used measures of intelligence, and the scoring system is calculated using standard deviation.

Slide 8: Distribution of IQ Scores
If we plot a frequency distribution of IQ scores in a population, it looks like this, with most people scoring 100 and a reliable spread of scores around this midpoint based on the standard deviation. This shows the number of standard deviations above and below the mean, each standard deviation corresponding to 15 points in the IQ score.
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About 68% of the population is within 1 standard deviation above or below the mean of 100, which works out to a span of IQ scores from 85 to 115.
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About 95% of the population is within 2 standard deviations above or below the mean – so between 70 and 130 –
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while pretty well everyone falls within 3 standard deviations, so between 55 at the low end and 145 at the high end. So, one sensible conclusion that we can draw from this is that if someone’s score places them at one of the extremes, say 160, we can be confident, in terms of IQ, that they are rare. Of course, this does not tell us that IQ is a valid measure of intelligence, that’s a whole other debate, but what it does tell us is that IQ, as measured by modern intelligence testing, is fairly reliable. So far we’ve focused on descriptive statistics, or displays of data. We can also use data to make inferences or conclusions, which is called inferential statistics.

Slide 9: Inferential Statistics
Inferential statistics allow us to make inferences or predictions about a population, based on observations of a sample. The fact that inferential statistics enable predictions makes it very powerful but these aren’t crystal ball predictions. Inferences are instead based upon mathematical calculations, which we won’t get into in great detail but it’s worth reviewing some important concepts. Basically, the idea underlying this is that we usually can’t test absolutely everyone we’re interested in. If we’re interested in human beings in general, then we could try and test all of the humans on planet earth, and the handful of people working on the international space station. That would give us everyone and we could be sure that our data represent humans as a whole. But for a bunch of obvious reasons, this isn’t possible. There are just too darn many of us and we’re all pretty busy. So what researchers do is to take a sample of the population to test, and then make inferences or predictions about the population as a whole. The term used most often to describe inferential statistical findings is statistical significance,
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a conclusion based on statistics that allows researchers to determine whether they can reject the null hypothesis. The null hypothesis is usually a statement that there’s “no difference”, and is typically the opposite of what the researcher hopes to find.
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Statistical significance is usually expressed as a p-value, and the conventional cut-off for a p-value is less than 0.05 or 5%. Let’s look at an example to show how inferential statistics are used in psychology.

Slide 10: Using Inferential Statistics
This study done at the University of Manitoba tested the effect of attributional retraining on grades in a first year introductory psychology course. The intervention involved getting the students to practice rethinking how they explained academic failure, by shifting explanations from things that are difficult to change – I did badly on that quiz because I’m dumb – to those that are possible to change – I did badly because I didn’t study for that one, I’ll do better next time. Control students were assigned to a business-as–usual condition, with no rethinking training while the others in the rethinking condition had two brief training sessions where they learned “healthy” ways to think about poor performance. The students were not treated differently in any other way. Although the researchers were hoping to see an improvement in course performance with this rethinking training,
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the statistical null hypothesis is the default position that there is no difference between these two groups.
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The dependent variable they used in this study to look at the effect was the percentage of students who failed or withdrew from the course. What they found was striking,
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far fewer students in the rethinking group failed the course. The researchers backed this up with statistical analysis that yielded a p-value of less than 0.05, which is usually indicated with an asterisk.
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This means they found support to reject the null hypothesis that there’s no difference between the groups and so the authors can say with some confidence that their experimental manipulation did appear to improve overall course performance. If they designed their experiment well – which in my opinion they did – and their sample of Intro Psych students is representative of all Intro Psych students, we can generalize these findings more widely to this population.
Take home message, if you are faced with an academic setback, try to think of some adaptive ways to think about poor performance. Research, back up with statistics, shows that it does seems to help.

Slide 11: Statistical Measures
There you have it, a very basic introduction to some statistical measures used in research.

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Tricky Topic: Neuronal Structure

Slide 1: Neuronal Structure
Neurons are the building blocks of the nervous system, so a basic understanding of how they work is crucial to the study of thought, behaviour, and emotion.

Slide 2: Cells of the Nervous System
Before we talk about neurons, we’ll first give a nod to another important cell type: glial cells.
Glia cells are the support cells of the nervous system.
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The word glia in Greek mean “Glue”. This is because it was originally thought that glia were responsible for binding the nervous system together.
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There are lots of different types of glia cells and they come in a variety of shapes and sizes.
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One type, called an astrocyte, gets its name from its star-like appearance.
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Astro is Latin for star. Astrocytes have widespread functions: they provide structural support, they’re a source of glucose for neurons when they’re hungry (and neurons are ALWAYS hungry), and they regulate ions and extracellular neurotransmitter levels (which are essential for signalling).
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Oligodendrocytes are another type of glia cells, however, their function is more limited than astrocytes. They make MYELIN, a fatty substance that wraps around and insulates a part of the neuron called the axon. Oligodendrocytes are the main myelinating glial type in the Central NS (so the brain and spinal cord) while
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Schwann cells serve the same function of wrapping around and insulating neuron axons, but in the Peripheral NS (so outside of the brain and spinal cord).
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Nerve cells are called neurons, and their job is to receive and send messages to both one another other as well as targets all over the body, so they’re our information processors.
Neurons are incredibly diverse in their shapes, functions, and communication targets. Generally speaking, neurons can first be categorized into two different types: first,
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those that project to distant targets outside of their local structure and second,
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those that project locally to targets within the same structure. Even further, neurons are vastly diverse within each of these general categories.
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Take for example three main structures of the nervous system: the cerebellum, the cerebral cortex, and the retina.
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In the top row you can see three major distant projecting neuron types: Purkinje neurons in the cerebellum; Pyramidal neurons in the cerebral cortex; and Retinal Ganglion Cells in the Retina.
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Now, take a look at the bottom row. Here are three examples of locally projecting neurons: Granule cells in the cerebellum, Basket cells in the cerebral cortex; and Bipolar cells in the Retina.
Understanding neuronal structure has been at the forefront of neuroscience research since it’s very beginnings with the pioneering work of Ramon y Cajal in the late 1800s. Still to this day, understanding neuronal structure serves as key factor in understanding the diversity and functions of the nervous system. Now that we understand the importance of neuronal shape, let’s take a closer look at how we describe the cellular structure of a typical neuron.

Slide 3: Neuronal Structure
Despite their diversity in size and structure, neurons all share common features. The soma,
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also called the cell body, contains the nucleus, and other cellular machinery necessary for the housekeeping functions that all cells need to maintain.
Extending from the soma
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are highly branched structures called dendrites, whose main function is to receive messages from other neurons. As we saw in the last slide, dendritic complexity can differ a lot depending on the neuron type. Neurons with many dendrites will have large total dendritic surface areas, which means they can receive many inputs from many other neurons. Amazingly, some individual neurons have been shown to receive as many as 10 000 inputs on their dendrites.
Also extending from the soma is the neuron’s axon,
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which can be thought of as the neuron’s highway to its targets. In this case the target is another neuron, but it could also be a muscle or a gland.
When describing the connection between two neurons we refer to the neuron sending the signal as the presynaptic neuron
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while we refer to the neuron receiving the signal as the postsynaptic neuron.
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Neuronal signals, or messages, are most often passed on to the next neuron by neurotransmitters, which are chemical signals typically released at the axon terminals
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of the presynaptic neuron and received by receptors on the dendrites of the post-synaptic neuron. It is important to note, that while most axon terminals synapse on dendrites, like you see here, axon terminals can also synapse onto other parts of the neuron, such as the soma and axon.
The contact points between the presynaptic axon terminals and the postsynaptic dendrites are quite tiny, but if we zoom in a bit closer, we can see much more.
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At this magnification, we can see little bubbles called SYNAPTIC VESICLES,
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and inside these you can see neurotransmitter molecules.
If we focus in now at the tip of the axon terminal
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we see vesicles releasing their neurotransmitter contents into the space between the terminal of the sending neuron and the dendrite of the receiving neuron.
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This space is called the synaptic cleft. The liberated neurotransmitter is then able to bind to receptors
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on the other side of the synapse and pass the message on to the next neuron.
Thus, the arrangement of neurons in relation to the synapse gives us the terminology to describe the direction of information flow.
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This is why we call the sending neuron, the presynaptic neuron, as it is found before synapse, and the receive neuron as the postsynaptic neuron, as it is found after the synapse. Although this seems fairly straightforward, so far we’ve been looking at simplified schematics; real synapses are a bit messier. Let’s have a look.

Slide 4: Synaptic Structure
This image was taken with an electron microscope and shows the structure of the synapse in the fly brain. It was by Nancy Butcher, a former neuroscience student who completed her Bachelor’s and Masters degrees at Dalhousie University. The synapse itself can be identified by the dark staining, representing high electron density.
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The arrow shows the location of the presynaptic neuron, which is easy to locate because there are lots of little bubbles,
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which are the vesicles containing neurotransmitter. The asterixis show the postsynaptic contacts, and this example the presynaptic neuron makes synaptic contact with, not 1, not 2, not 3, not even 4, but FIVE separate dendrite branches. So even at a single terminal there can be lots of places for neurons to communicate with one another.

Slide 5: Three Types of Neurons
If we classify neurons based on their synaptic connections, it yields THREE different types.
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Sensory neurons receive their input from various stimuli in the environment. They tend to have very specialized shapes in order to capture sounds, sights, smells, and other types of information we get from our sensory world. For example, in this reflex arc
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we have cutaneous sensory neurons
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that transmit the sense of ‘touch’ from the skin into the spinal cord.
The second neuron type
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are interneurons, and they receive their input FROM and send their output TO, other neurons, so their communication is exclusively with other neurons.
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Interneurons are responsible for all the tasks that don’t involve direct sensory input, or direct motor output. Back to our cutaneous reflex arc, interneurons are located in the spinal cord
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and receive inputs from the sensory neurons. They then make connections with other neurons in order for the sensory messages to get transmitted to the brain.
The final neuron type are
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motor neurons. Motor neurons receive innumerable inputs from neurons in the brain, spinal cord, and periphery. They are located within the central nervous system and send signals to both muscles and glands throughout the periphery.
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Thus, they function to regulate not just movement, but also hormone release.
Again, coming back to our example, Motor neurons are the final link in the reflex arc.
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They receive inputs from upstream interneurons and send signals to peripheral muscles. Thus, the effective communications between sensory neurons, interneurons and motor neurons allows our nervous systems to both sense and respond to our dynamic environments.

Slide 6: Neuronal Signalling: Dendrites to Axon Terminals
So far, we have discussed how signals are chemically transmitted across the synaptic cleft from one neuron to another. Further we have discussed how to classify neurons based on their input and output targets. However, as you may have noticed, the distance between where a neuron might receive a signal, at its dendrites, and where it releases a signal, at its axon terminals, can be very large. In some cases, this distance can be over a meter! For example, think about motor neurons in your spinal cord.
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A single motor neuron may have its dendrites in the spinal cord
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and its axon terminals all the way down your leg signalling in your calf muscles.
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Thus, the question is raised, how are signals transmitted from a neuron’s dendrites and soma to its axon terminals? The answer lies in the remarkable electrical properties of all neurons.

Slide 7: Electric Properties of Neurons
Neurons are different than most other cell types because they can transmit electrical signals along their membranes.
Electrical current in neurons is carried by ions, which are particles that carry a positive or a negative charge. Each Ions has a CONCENTRATION GRADIENT, which means that ion may have different concentrations on each side of the neuronal cell membrane.
The difference in ion concentrations is made possible by ion pumps, which use energy to maintain the unequal distribution of ions on either side of the membrane. Because of the different concentrations of ions, there is also an ELECTRICAL GRADIENT, which is a term that refers to the difference in CHARGE across the neuronal membrane. If you stick an electrode into a typical neuron to measure the electrical properties at rest (when it’s not active), you’d find that the inside is slightly more negative than the outside.
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This is called the resting potential and in a typical neuron is -70mV. Let’s look at the concentration of different ions across the neuronal membrane.

Slide 8: Distribution of Ions
There are many ions in a neuron, but these are the major players involved with electrical signalling.
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First are large negatively charged proteins, which are represented by the symbol A- and are predominantly found inside the neuron.
Next, Chloride,
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or Cl- carries a negative charge and are located mostly outside the neuron.
Now let’s look at some of the major positively charged ions. First, Potassium
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is a positively charged ion, represented by the symbol K+, and found mainly inside the neuron.
Unlike potassium, positively charged Sodium,
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represented by the symbol Na+ is found mostly outside the neuron.
Lastly, Calcium,
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or Ca2+, carries a DOUBLE positive charge, and are more abundant outside of the neuron.
This different distribution of ions is important for the electrochemical gradient, and that’s necessary to provide the driving force for ion movement. Ion movement is ESSENTIAL for the two important jobs of neurons which enable the signaling from their postsynaptic receptors and then along their axons to their axon terminals…

Slide 9: Neurons have two important jobs:
The first job is to transmit a message from the presynaptic neuron, across the synaptic cleft, to the post synaptic neuron.
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This is achieved by converting a chemical neurotransmitter signal in the synaptic cleft, into an electrical signal in the neuron.
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This occurs at the location in the neuron where it receives synaptic inputs, which is usually in its dendrites.
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This is a type of signal called a graded potential.
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The second important job of neurons, after receiving a message, is to transmit that message along its length
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from its dendrites to its axon terminals. This happens via a type of electrical signal called an
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action potential.

Slide 10: Neuronal Communication
Our neurons are talking to each other all the time, by the millions and millions! Try and picture that – it’s mind-boggling. Well, fear not,
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with this figure we’ll outline the two types of electrical signalling, using a simplified circuit of just three neurons. Using this circuit well attempt to show the repetitive nature of the signalling processes. First, we’ll start our signalling process with an action potential
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in the first neuron. This action potential propagates down the axon of the first neuron until it reaches the axon terminals. Once it has reached the axon terminals it initiates Neurotransmitter release
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into the synapse between the first neuron and the second neuron. These neurotransmitters are then received by the dendrites of the second neuron producing GRADED Potentials.
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Once these grade potentials reach a certain threshold, they initiate another action potential, but this time it’s in the second neuron.
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As we saw before, the action potential propagates down the axon of the second neuron
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until it reaches the axon terminals, again, initiating neurotransmitter release.
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Now, neurotransmitter is released into the synapse between the axon terminals of the second neuron and the dendrites of the third neuron, which again, initiates grade potentials, except this time in third neuron.
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This process then repeats
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onto 4th, 5th, 6th, and millions of other neurons.

Slide 11: Neuronal Structure
Knowing the structures of neurons and signalling types in neurons are important first steps in understanding their functions. Ultimately, the output of the nervous system, which governs our movements, thoughts, and behaviours, are determined by how different neuron types send and receive signals with one another.

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Tricky Topic: Synaptic Transmission

Slide 1: Synaptic Transmission
To understand how neurons communicate with one another, it is vital to understand the basics of synaptic transmission.

Slide 2: Neuronal Communication
The nervous system has billions of neurons, and each of them can have hundreds or thousands of contacts. These neurons are in constant communication, even when we’re sleeping. This sheer amount of activity is truly remarkable. Despite this, neuronal communication is made possible by a couple of different types of electrical signals, which are linked by chemical messengers. Let’s zoom in for a closer look.
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Neurons have two important jobs: One is to transmit a message to a target across a synapse,
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using neurotransmitters as messengers.
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The type of electrical signal resulting from this is called a GRADED POTENTIAL.
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If the graded potential is the right size and type then it allows the neuron to do its second important job, which to carry the message along the length of its axon to its target using a type of electrical signal called an ACTION POTENTIAL.
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When an action potential reaches the axon terminals
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it triggers neurotransmitter release,
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which continues the cycle of producing a graded potential and then an action potential in the next targeted neurons.
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This continuous cycle of communication is running all the time in your nervous system. For this Tricky Topic, we’ll focus on the events at the synapse and learn how synaptic transmission plays a role in neuronal communication.

Slide 3: Pre- and Post- synaptic
We’re going to start our journey to the synapse with a bird’s eye view. The axon terminals
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of the neuron on the left, shown here in red, form synapses with the dendrites of the neuron on the right. Although most neuronal axon terminals synapse on dendrites, like you see here, keep in mind they can also form synapses on other parts of the targeted neuron, such as the soma and the axon. The sending neuron on the left is referred to as the presynaptic neuron
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and the receiving neuron on the right is referred to as the
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postsynaptic neuron. Keep in mind these are relative terms. Most neurons act as senders AND receivers of information, so they’re both presynaptic and postsynaptic, depending on which event we’re referring to. Let’s pick this particular synapse and zoom in for a little more detail.
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At this magnification, we can see little bubbles called SYNAPTIC VESICLES,
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and inside these you can see neurotransmitter molecules.
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These vesicles here are releasing their neurotransmitter contents into the synaptic cleft. Once released into the synapse, the neurotransmitters can travel the short distance to the postsynaptic neuron.
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Once they reach the other side, neurotransmitters bind to receptors on the postsynaptic neurons.
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There are lots of different types of receptors, but the simplest ones are gated to ion channels, like shown here. Once the neurotransmitter binds, it opens the ion channel part of the receptor allowing certain ions to travel across the neuronal membrane along their electrochemical gradient.
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This influx of positive current, in the form of positive ions, is what generates GRADED POTENTIALS
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in the postsynaptic neuron. Thus, through the binding of postsynaptic ion-channel receptors, synaptic neurotransmitters initiate postsynaptic graded potentials.

Slide 4: Steps in Synaptic Transmission
Let’s review the steps so far: First,
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neurotransmitter is released from the presynaptic terminal. Second, that neurotransmitter binds to the receptors
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opening up their ion channels on the postsynaptic side.
What happens next in the postsynaptic neuron depends on the type of ion channel receptor that is activated, as different receptors are permeable to different types of ions. The type of ion channel receptor that is activated will then determine the type of graded potential that is initiated.
If the channel opens and positive ions enter through the channel,
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then the inside of the neuron will become less negative. For example, the potential of the neuron might rise form its resting potential of -70 mv to -55 mv.
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This is referred to as a DEPOLARIZATION
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and is considered excitatory.
If instead negative ions enter through the channel, then the inside of the neuron will become more negative.
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For example, the potential of the neuron might decrease from its resting potential of -70 mv to -90 mv.
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This is referred to as a hyperpolarization
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and is considered inhibitory.
Let’s look at some examples of different types of receptors which produce either excitatory or inhibitory graded potentials.

Slide 5: Depolarization (+)
First let’s look at depolarization. A neurotransmitter that is always excitatory at its synapses is glutamate,
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so we can pretend that the orange diamonds are glutamate molecules, and the white circles in the synapse are sodium ions.
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When glutamate binds to its receptor
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the channel opens and sodium ions are driven by their electrochemical gradient to enter the neuron.
When sodium moves into the cell through the receptor ion channel, it brings its positive charge with it, making the cell more positive,
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which is called a depolarization. If the channel remains open for longer, more sodium will flow in,
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making the cell even more positive.
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This type of graded potential is called an excitatory postsynaptic potential,
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or EPSP for short.

Slide 6: Hyperpolarization (-)
What about hyperpolarization? A neurotransmitter that’s almost always inhibitory at its synapses is GABA,
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and its receptor channel is permeable to negatively charged chloride ions, shown here as black circles.
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When GABA binds to its receptor, the channel opens and chloride ions are driven into postsynaptic neuron because of their concentration gradient
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When chloride moves into the cell through the GABA receptor ion channel, it brings its negative charge with it, making the cell more negative, which is called a hyperpolarization.
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If the channel remains open for longer, more chloride will flow in,
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making the cell even more negative.
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This type of graded potential is called an inhibitory postsynaptic potential,
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or IPSP for short.
So why does this matter?

Slide 7: Steps in Synaptic Transmission
Well if the postsynaptic neuron adds up all of the EPSPs and IPSPs and the membrane potential reaches a threshold
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of -55mV, a different type of ion channel comes into play, one that is opened by a change in voltage.
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The ion channels we’ve learned about so far are opened by neurotransmitter binding, but these VOLTAGE-DEPENDENT sodium channels are sensitive to changes in charge. At resting conditions, say -70 mV,
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these channels are closed and Na+ ions cannot pass through them into the cell
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However, when the sum of all EPSPs and IPSPs raises the neurons potential above -55 mV,
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the voltage-dependent sodium channels open allowing Na ions into the cell
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When these voltage dependent sodium channels open, they create an action potential, which allows the neuron to send the message to its target.

Slide 8: Synaptic Transmission
Overall, synaptic transmission may seem quite tricky, but it’s actually quite simple once you know the basics.

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Tricky Topic: Action Potentials

Slide 1: Action Potentials
Neurons communicate with each other using the language of electrochemistry, and to appreciate how information is transmitted across large distances, in some cases over a meter, it’s necessary to understand how action potentials work. But first let’s review the basics of neuronal communication.

Slide 2: Neuronal Communication
Neurons have two important jobs.
One is to transmit a message to a target across a synapse
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and the other is to carry a message along the length of its axon
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to the next neuron. The first job
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is made possible by neurotransmitters released from the presynaptic neuron. They trigger graded potentials
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in the postsynaptic neuron, which come in two flavours, excitatory postsynaptic potentials (or EPSPs)
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and inhibitory postsynaptic potentials (or IPSPs)
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The neuron has the ongoing task of adding up all the EPSPs and IPSPs, to determine when to start the neuron’s second job of carrying the message down the length of the axon. If the membrane potential reaches its threshold of -55mV,
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a type of electrical signal called an ACTION POTENTIAL
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is generated. The action potential then triggers neurotransmitter release once it reaches the terminal,
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and the process starts all over again in a new neuron

Slide 3: Action Potential Initiation
Although an action potential is first generated where the membrane potential reaches -55mV, which is usually in the axon initial segment right at the soma, we’ll focus on the events in the axon, since their main job is to propagate the action potentials to the neuron’s targets at the terminals.
The firth step of an action potential is the opening of voltage-gate sodium channels. As a post-synaptic neuron receives Neurotransmitter signals, if the threshold of -55mV is reached, a special type of sodium channel, that’s sensitive to electrical changes, gets open.
Let’s take a quick look at how different receptor types distribute in the neuron.
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Unlike the receptor channels in the synapse
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that are neurotransmitter gated, that is, they open in response to specific neurotransmitter binding, voltage-dependent sodium channels,
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which are most densely located in the axon, open when the membrane potential is depolarized to -55 mV.
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In a resting neuron there are more sodium ions outside the neuron than inside, so there’s a chemical AND electrical imbalance that promotes sodium movement INSIDE the cell.
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Thus, when voltage-dependent sodium channels open, sodium rushes into the neuron, bringing its positive charge, making the cell even more depolarized.

Slide 4: Action Potentials & Axon Structure
Once an action potential is initiated it propagates along the axon to the terminals.
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If we think about the nervous system as a whole, hundreds of millions of action potentials are being fired on top of one another at all times. Thus, the nervous system must operate within a remarkably sensitive computational time frame. Indeed, some action potentials can travel at speeds up to 100m/s. One strategy the nervous system uses to increase action potential speed to as quick as possible is the surrounding of axon shafts with the fatty membranes of glia cells. In the central nervous system, oligodendrocytes form fatty Myelin Sheaths along axons,
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as seen here. This insulates the axon allowing electrical charge to quickly jump
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between Myelin within the axon. The spaces between the myelin Sheath are referred to as,
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Nodes of Ranvier. If we zoom into a Node of Ranvier,
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we can see this area is densely clustered with ions channels, which allow the passage of electric charge, in the form of ions, across the axon membrane in areas not covered by myelin.

Slide 5: Action Potential Spread
Let’s now take a closer look at the mechanisms behind an action potentials travel down the axon away from the soma to the axon terminals.
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Here we can see a neuron with its axon
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extending away from its soma. If we take a cross section
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along the length of its axon and zoom in we can start to appreciate what’s happening inside the neurons axon. When the graded potentials at the synapse add up to -55mV
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this is detected by the voltage-dependent sodium channels
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which are found in large numbers along the axon. As the voltage gated sodium channels open, sodium rushes into the axon
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along its electrochemical gradient, bringing its positive charge into the neuron. This depolarization is then sensed by neighbouring sodium channels
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which also open when the membrane potential reaches -55 mV, having sodium ions and positive charge rush into the neighbouring region of the axon.
At this point, if we were to stick an electrode into the neuron
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we would see the membrane potential rise at the location where the sodium channels are opening. At this first time point this location is proximal to the soma, that is, it is closer to the soma than the terminals.
The wave of depolarization makes its way down the axon,
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as neighbouring sodium channels along each part of the axon open allowing sodium to continue to flow in
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This depolarization wave travels in proximal to distal direction.
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At a time point, 2, if we were to again stick an electrode into the neuron
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the depolarization would be measured farther down the axon.
This process of sodium channels bringing positive charge, which then opens adjacent voltage-dependent sodium channels, works its way uninterrupted all the way down the length of the axon. So once an action potential gets started, it doesn’t stop until it runs out of neuron.
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To be completed at a later date (updated to 6:44)

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Tricky Topic: Cortical Anatomy

Slide 1: Cortical Anatomy
This image is easily recognizable as a human brain, but this is a simplified, colour-coded version.
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The actual human brain is a little messier and looks a bit like this.
A huge amount is devoted to the cerebral cortex, which is most what you can see when you look at an intact human brain. Upon first glance it doesn’t appear to have much in the way of organization.
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If you compare it to a street map of Edmonton, there certainly doesn’t appear to be a lot of urban planning going on in the cortex. However, the cortex has been mapped and described in astonishing detail. At this point, the picture is still far from complete, but neuroscientists continue to piece it together.
For this Tricky Topic, we’ll consider the arrangement of structures and connections in the cortex. Before diving in, it’s first helpful to consider where this human cortex came from.

Slide 2: Human Brain Evolution
Some evidence for the origins of the human brain comes from comparisons to our early ancestors. Over on the far right
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is a skull of the Sahelanthropus tchadensis, which lived between 6 to 7 million years ago. Some argue this species might be our earliest ancestor.
Although their skulls resemble chimpanzees and their brains are estimated to be only a quarter of the size of modern humans, they share some anatomical features that suggest they walked upright.
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A later human ancestor is the Australopithecus afarensis, who lived in Africa from 2 to 4 million years ago. The most famous member of this species is Lucy,
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a female whose remarkably intact remains survived until discovery in 1974. Her brain was a little larger than Sahelanthropus, about 1/3 the size of the modern human.
Homo erectus,
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who hung around on earth for a million and a half years or so, had an estimated brain capacity much larger than Lucy’s.
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The more modern Homo Neanderthalensis, the species that most people think about when they picture cavemen, had a very large brain. Neanderthal skulls differed from other early humans in that they had a prominent ridge on their forehead
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shown here.
The brains of modern humans, Homo Sapiens, are actually thought to be a little bit smaller than those of Neanderthals but are amongst the largest of the hominids. Homo sapiens’ behaviour is responsible for our biological success.
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We can choose to wear a hijab and drink a coffee while taking a selfie. Other animals don’t do these things.
The flexibility and adaptability of human behaviour is driven by our large, unique brain. We can only estimate what the brains of our relatives looked like because we have remains of skulls, not actual neural tissue. We can get some sense about the anatomy and function of the human brain by comparing to other living species.

Slide 3: Comparing Species
At first glance, this rat brain on the far right looks much smoother than the chimpanzee and human brains, which appear more folded and wrinkly. This folding allows a large amount of brain to be scrunched together into a small space. You can see how this works for yourself if you take a sheet of paper and crumple it up.
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More brain folding is thought to represent more brain matter. Primates, like humans and chimps shown here, have large brains with lots of folding in the cortex, and this is thought to underly some of the fundamental differences in thought and behaviour.
Let’s take a peek inside the human brain.

Slide 4: The Human Brain: A Peak Inside
Neuroscientists have been able to piece together an overall organization of the brain as shown in this cross section. This organization roughly divides the brain into three main regions,
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the hindbrain just above the spinal cord, the midbrain in the middle, and the forebrain at the top. Clearly most of the brain is forebrain, and most of THAT is cortex, a structure that makes up about 80% of the human brain.
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Because the human cortex is so highly folded, it resembles a pile of worms.
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However, the word “cortex” actually means bark in Latin,
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since it covers the rest of the brain just like bark covers a tree.
So what does the cortex do? The cortex is responsible for all sorts of complex thought processes like
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perception, decision-making, and language. Let’s take a look at the human cortex in more detail.

Slide 5: (No Title – Blue Brain on dark background)
The cortex is made up of two hemispheres: left and right.
We’re looking at the left hemisphere right now, but
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if we rotate the brain, we can see that the right hemisphere is the same size and shape.

Slide 6: Anatomical Divisions
Each hemisphere has four lobes: the very front is the frontal lobe,
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behind it, the parietal lobe,
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in the back is the occipital lobe, and near the temple, resembling the thumb of a boxing glove is the temporal lobe.
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Of course, a real brain is not colour-coded,
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but it’s still possible to identify these general areas.
Just looking at the cortex and its arrangement doesn’t necessarily tell us what each of these areas actually do. Figuring out the functional divisions of the cortex requires different strategies.

Slide 7: Three Functional Divisions
There are three main functional divisions of the cortex.
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Primary sensory areas are the first bit of cortex that receive incoming information from our sensory organs.
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There is a primary sensory area in the cortex for each of our senses, and most of this is relayed through the thalamus,
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which sort of acts like a switchboard.
These primary sensory areas are important for categorizing and the integrating sensory information, which are the first steps in conscious perception.
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The primary motor area is the strip of cortex at the posterior or back end of the frontal lobe. It receives information from surrounding areas and initiates a motor plan for voluntary movement
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by communicating with motor neurons in the brainstem and spinal cord.
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Association cortex, which makes up most of the cortical volume, has a less well-defined job description. It integrates information gathered from other areas to regulate complex thought processes
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such as problem-solving, decision-making and language.
Unlike the primary sensory and motor areas, electrical stimulation of association cortex does not produce movement or sensation. For this reason, it is sometimes referred to as “silent” cortex.
Now you might be thinking: under what circumstances would somebody sign up to have their brain stimulated in the first place? Well that’s a good question, and the answer is that this happens in unusual circumstances.
Some medical procedures have allowed neurosurgeons to take a really intimate peek inside the brain.

Slide 8: A Deeper Peak Inside the Brain
From the 1930s to the 1950s,
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neuroscientist and neurosurgeon Wilder Penfield made incredibly detailed observations from awake, locally anaesthetized patients undergoing surgery for epilepsy.
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Penfield tickled the neurons with a mild electric current
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and the patient then reported their sensations and movements which were recorded and mapped.

Slide 9: Electrical Stimulation in Epilepsy Patients
When Penfield stimulated the brain along the strip of the cortex shown in red,
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his patients reported movement on the opposite side of the body. When he stimulated the strip shown in green,
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they reported sensations of touch, again on the opposite side.
These careful observations allowed him to map the primary motor cortex and primary somatosensory cortex. Somato means ‘body’, so somatosensory is a fancy term for body sense, or touch.
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With repeated stimulation over many patients, Penfield notices the arrangement of body parts in these strips of cortex is the same as in the body itself
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The feet at one end and the head at the other but for the opposite or contralateral
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side of the body.

Slide 10: Primary Motor & Somatosensory Maps
If we take a slice from the primary motor area from one hemisphere you can see that the body map in the cortex is the same as in the actual body,
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with the feet at one end and the head at the other.
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If we look at the somatosensory cortex right next door, we can see a similar body map for touch. Note the disproportionate representation for some body parts like the hands and face.
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For instance, the fingers take up a lot of space compared to the legs.
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So the amount of brain devoted to a body part depends on its function rather than its physical size. We have much finer motor control of the muscles in our fingers compared to our legs, so the fingers get more real estate in the motor cortex. The same is true for touch sensitivity of these body parts, so they take up more of the somatosensory cortex.
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Some organs, such as the teeth, gums and genitals have representation in the somatosensory map but not the motor map. Of course, these areas have extreme touch sensitivity, but not much in the way of motor control.
Penfield’s stimulation experiments reveal the organization of the motor and touch maps in incredible detail, but opportunities for this type of research study are rare. Another way scientists learn about functions of the cortex is by making observations of people who have sustained some sort of damage, usually through disease or injury.

Slide 11: Learning from Injury
This image outlines what happened to 25-year old Phineas Gage, an American railroad construction foreman who suffered from an accident in 1848 in which a tamping iron, used to compact explosives into holes drilled in rock, set off a spark causing an explosion that sent the tamping iron through his head.
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He sustained extensive damage to his frontal lobes, especially his prefrontal cortex.
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After he recovered from the initial trauma, he showed profound behavioural changes and he became impulsive, impatient and disrespectful, using profanity, which is unlike him before the accident. He lost his job because the railroad felt he could no longer perform his duties.
This is one of the most famous case studies of brain injury and since then research has pointed to the frontal cortex, especially the prefrontal cortex, as being particularly important in planning and impulse control.
With these early attempts as well as more modern, and less invasive techniques such as neuroimaging, scientists have been able to localize certain functional areas of the cortex to particular anatomical locations.

Slide 12: Cortical Lobes: Summary
As we learned from Phineas Gage,
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the frontal lobe is involved in attention, planning and impulse control, and has a large role in voluntary movement
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since it houses the primary motor area.
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The parietal is involved in sensation and perception of touch,
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since it’s here you can find the primary somatosensory area.
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The occipital lobe in the back is strongly tied to vision
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and houses the primary visual cortex.
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The temporal lobe has a strong role in hearing,
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and is the location of the primary auditory cortex, which receives incoming information about sounds.

Slide 13: Cortical Anatomy
Keep in mind that this is a brief description of cortical anatomy and does not include all of the functions of the cortex, in fact we’re still learning about it.

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Tricky Topic: Hemispheric Lateralization

Slide 1: Cortical Lateralization
Although the left and right sides of the human cortex look almost identical, the hemispheres have specialized functions.
You might have heard that the left brain is analytical and logical while the right is more intuitive and creative.
The idea that people are either left-brained or right-brained is very popular, but it turns out, thankfully, that we use our whole brain, we just recruit the left and right hemispheres for different tasks, a phenomenon known as cortical lateralization. Let’s explore this in more detail.

Slide 2: Brain & Body Connections
This woman is facing us so her left is on our right, and vice versa.
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The primary motor cortex, which controls voluntary movement,
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is located roughly here.
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We know from work of German physiologist Eduard Hitzig in the 1860s, that this part of the brain has a CONTRALATERAL connection to the body parts it controls, which means that it is connected to the OPPOSITE SIDE.
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Hitzig first noticed this while caring for wounded soldiers, he found that touching the surface of this specific strip of the cortex caused movement on the OPPOSITE side of the body.
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The various primary sensory areas also have this CONTRALATERAL organization such that incoming sensory information from the body is sent to the cortex on the opposite side.
The primary somatosensory cortex is located just behind the motor strip
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which is responsible for the perception of touch sensations,
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receives its information from sensory neurons whose axons cross over,
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so that the right side of the body talks to the left somatosensory strip, and the left side of the body talks to the right.
The connections of these primary sensory and motor areas of the cortex are also SYMMETRICAL,
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in that the left and right sides of the body have equal representation in their respective hemispheres.

Slide 3: The Visual Pathway
Let’s consider the organization of information from the visual system to the cortex. Unlike the somatosensory system, which sends signals separately from each side of the body, the visual system is a little different because the left and right eyes capture images from BOTH the left and right sides of visual space, as shown in this figure.
For example, the outside part of the right eye
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and the inside part of the left eye
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detect stimuli in the left visual field, shown in red.
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The pathway from the inside part of the left eye crosses over at the optical chiasm, and the signals then get sent to the right hemisphere.
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The pathway from the outside part of the right eye stays on the same side,
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so ultimately the signals from left visual world ALL end up in the right hemisphere. If you follow the green lines you can see that this same arrangement is true for the right visual field.
In other words, the information from left and right visual space is sent to the primary visual cortex on the opposite side, in a way that conserves the symmetry of the visual scene.

Slide 4: Association Cortex
Unlike the primary sensory and motor areas, the association cortex is asymmetrical
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because its functions differ between the left and right hemispheres. The left hemisphere appears to have a stronger role in processing language and logical based thought,
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while the right is involved in more holistic, spatial-type tasks.
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Most people, about 95% of right handers, and 85% of left handers, show this bias, although a small proportion of people have the opposite arrangement.

Slide 5: Corpus Callosum
Regardless of whether the lateralization is typical or reversed, ordinarily our hemispheres communicate with each other via a large bundle of axons called the corpus callosum
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located here in the middle of the brain.
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This highway allows for the exchange of information between the hemispheres.
But how do we know about association cortex asymmetry or the role of the corpus callosum?

Slide 6: Cortical Lateralization
The asymmetrical distribution of function in the association cortex is called cortical lateralization. A lot of what we know about lateralization comes from observations of people with split brain syndrome
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who have had the corpus callosum cut. Believe it or not, this is a condition caused by surgeons, in extreme cases, as a last resort treatment for epilepsy.
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Epilepsy is characterized by excessive electrical activity in the brain,
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which can spread across large areas.
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Severing the corpus callosum can prevent the spread of troublesome electrical activity and confine the seizure to one area.
One consequence of split brain surgery is that stimuli from the various sensory systems can be sent separately to each hemisphere. Recall how sensory information is conserved in a CONTRALATERAL and SYMMETRICAL way. So in the visual system,
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the bits of the eye that capture left visual space are sent to the primary visual cortex in the right hemisphere
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and vice versa. Because the corpus callosum is cut in split brain patients, the hemispheres can’t transfer information to each other.
So what happens to people who have this procedure? As it turns out, people generally function just fine under everyday conditions.

Slide 7: Split Brain Syndrome
You can notice a difference in information processing under controlled laboratory conditions where the split brain patient keeps their head stationary and the researcher presents visual and tactile stimuli separately to each hemisphere.
What research has shown is that people with split brain syndrome,
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can easily verbally identify something presented in their right visual field, since this information travels to the language-intensive left hemisphere.
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However, when something appears in the left visual field,
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which travels to the spatial, non-verbal right hemisphere,
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they cannot name it.
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If instead they are given a SPATIAL identification task that is confined to the right hemisphere, such as identifying an object with their left hand by touch, they can easily retrieve it,
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even though they can’t NAME what they just saw.
This demonstrates that the left and right hemispheres, if they can’t talk to each other, are very limited in what they can do.

Slide 8: Brain Damage
Another source of information about cortical lateralization and asymmetry comes from studies of people who have sustained injury to particular regions of the association cortex.
We can’t cover all of the brain damage studies – there are simply too many – but we can look at some areas in particular in the left and right hemispheres whose damage results in specific types of impairments.
Two examples we’ll consider are aphasias,
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which are impairments in language comprehension usually as a result of damage to the left association cortex,
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and agnosias,
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which are perceptual impairments resulting in difficulty in recognizing objects or people from their sensory features and are usually a result of damage to the right association cortex

Slide 9: Aphasias
Broca’s aphasia, first described by the French physician Paul Broca,
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is characterized by difficulty producing speech although speech comprehension is mostly unaffected.
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Broca examined these patients’ brains after they died and discovered damage to an area in the left frontal lobe,
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located near the primary motor cortex,
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which became known as Broca’s area.
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Wernicke’s aphasia, first described by German physician Carl Wernicke,
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is characterized by few problems producing the movements to speak, but speech doesn’t make sense and patients have difficulty understanding others. Upon examination of their brains, they were found to have damage to an area in the left temporal lobe,
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quite near the primary auditory cortex,
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involved in hearing.
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This area became known as Wernicke’s area.
Whereas aphasias are usually associated with damage to different parts of the left association cortex – often through injury or stroke – agnosias are most commonly found in people with damage to parts of the right association cortex.

Slide 10: Agnosias
Agnosias are very specific perceptual issues, unrelated to any problem with the eyes or with vision in general, but rather in dealing with processing incoming visual information and making spatial sense out of it.
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Contralateral neglect is an unusual condition where people ignore the left side of their world. Dressing only the right side of the body or eating from only the right side of one’s plate are common symptoms.
Keep in mind that the right association cortex is specialized in spatial tasks,
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and this disorder is linked to damage in the right parietal cortex.
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Prosopagnosia is an even more unusual condition, also known as FACE BLINDNESS.
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People with prosopagnosia have difficulty identifying specific faces, even though they have no trouble seeing faces.
Face recognition is a very specialized spatial task. Think about it. It is difficult to describe someone using our words, everyone has two eyes, a nose, couple of lips. It’s the differences in size, shape, and position of these features that allows us to tell the difference between our best friend and stranger who has the same colouring and general features.
This disorder is associated with damage to an area of association cortex that spans the occipital and temporal lobes called the fusiform area,
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and is tucked in behind the cortex here.

Slide 11: Cortical Lateralization
So association areas in the left and right cortices often show a bias towards particular types of functions. Before the development of brain imaging technologies, discoveries about cortical lateralization were made possible by careful observations of people with brain damage.

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Tricky Topic: Visual Transduction

Slide 1: Visual Transduction
Transduction refers to the conversion of one form of energy into another. In the nervous system, VISUAL transduction involves turning energy from photons of light into electrochemical neural signals. So let’s first look a bit more closely at the properties of light.

Slide 2: Light & the Electromagnetic Spectrum
Light is one type of electromagnetic radiation, carried by tiny particles called photons that travel all around us in waves. Although we’re not often aware of it,
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we’re surrounded by all sorts of electromagnetic radiation that vary along a vast spectrum of sizes. These different types of electromagnetic radiation have waves of different lengths so…
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…their size may be referred to as their wavelength. The largest waves are those that carry AC electricity
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which are about 1000m long, while the smallest are tiny gamma rays
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around 0.1 Angstroms, or one-100 billionth of a meter. Other waves between these two, such as radio and television waves, microwaves, and X-rays,
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are quite useful to us and are constantly around us throughout our lives. As you are probably aware though, we are unable to see any of these waves.
The reason that we humans can’t see these waves is that our visual systems can only detect a very narrow band in the electromagnetic spectrum.
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Humans are only sensitive to the wavelengths from roughly 380 to 740nm
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and so we call this range “visible light.”
We can see the components of white light if we separate the wavelengths with a prism,
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and within this range, we perceive different wavelengths as different colours. For example, we perceive blue when we’re presented with a 450nm wavelength, whereas we perceive red when we’re presented with a 700nm wavelength.
Interestingly, some animals can see other wavelengths. Rattlesnakes are known to detect infrared light,
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which are longer wavelengths than the visible human range. Snakes use this ability to find suitable shelter, detect predators and to find vulnerable prey. Some birds on the other hand, such as the European starling, can detect wavelengths shorter than the human visible spectrum, in the ultraviolet range.
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Many birds have colouring on their plumage that is only visible under ultraviolet light, meaning that birds likely see very different markings on each other, compared to what we see on them.
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Okay, now that we understand some of the properties of light across the electromagnetic spectrum, let’s look at what happens when the light enters your eye…

Slide 3: The Eye
This is a cross-section of the eye, so we’re looking at it from the side, through its center.
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Light begins its journey at the CORNEA,
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which is the transparent protective layer over the outside of the eye. Once light passes through the cornea it then travels through a small opening called the pupil,
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which is the dark circle in the center of the eye.
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The size of the pupil changes depending on how much light is in the environment: in dim light it dilates to become larger
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allowing more light in, while in bright light it constricts
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to let less light in. The opening of the pupil is adjusted by the iris,
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which gives the eye it’s characteristic colour. Some of the most common eye colours are brown, blue, or green.
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Directly behind the pupil
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is the lens, which is responsible for bending light to focus the image onto the retina. The thickness of the lens can adjust depending on how much the eye needs to focus. For example, if you wanted to focus in the distance on a tree,
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the lens would focus the light reflecting off the tree into the back of your eye.
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To change the focus of the lens for different distances and sizes, there are tiny muscles attached to either side of the lens that allow it to become either thicker or thinner depending the image.
Once the light has passed through the lens it then travels towards the back of the eye,
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it makes contact with the retina,
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which is a sheet consisting of a number of specialized neuronal cell types, which communicate with the rest of the brain via the Optic Nerve.
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It’s here that transduction occurs, so let’s look a little bit closer at the retina itself.

Slide 4: The Retina
If we zoom in on the retina, we can see it is composed of three different layers of cells. Although these cells are located in the eye, they’re actually neurons. The rod and cone cells at the back of the retina are sensitive to light, so they’re collectively known as PHOTORECEPTORS,
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and it’s here that light signals are converted into an energy form that the nervous system can understand: an electrochemical signal. One odd thing about the arrangement of the photoreceptor layer is that photons entering the eye have to travel across several other cell layers
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before they meet the rods and cones that understand their message. Because the rods and cones are the first step in visual transduction, we’ll first focus on what happens in these cells before introducing the other retina cell types.
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This is what rod and cone photoreceptor cells look like under an electron microscope. photoreceptors are a very specialized sensory cell. That is, they are designed to respond to specific incoming signals from the outside environment. So, in this case, these sensory receptors are specifically designed to respond to photons of light. When a light stimulus interacts with a sensory receptor it causes a change in the cell’s permeability to particular ions, which then affects the release of neurotransmitters.
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Let’s look more closely at these photoreceptors to see what happens INSIDE these cells when they interact with light.
If we focus in on the rod and cone cells
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we can see that although they have different shapes, they have very similar characteristics.
Both cells have terminals
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which synapse with the next layer of cells, a cell body
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containing the nucleus and other cell machinery, and an outer segment that contains discs of visual pigments
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This is the part of the rods and cones where photons of light begin the process of transduction.
If we look even more closely at the structure of these discs, we can see the chemicals that allow our eyes to convert light into neural signals.

Slide 5: Photoreceptors: Rods
In this rod cell
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the light-absorption happens in these discs.
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If we zoom in further to the lipid bilayer of the membrane
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we find a specialized membrane-bound protein known as opsin, shown here in colour.
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If you look in the centre of the opsin, you’ll notice a dark coloured molecule called retinal.
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Collectively, the retinal and opsin structure is known as rhodopsin.
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In the dark, the retinal is bound to the opsin in a very specific conformation, however when a photon of light makes contact with these component molecules, rhodopsin changes its conformation
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This leads to a change in the membrane permeability allowing ions to enter into the photoreceptor cell, thus, creating an electrical signal.
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Let’s remember that here, we are talking about specifically Rod photoreceptors and not cones.
Rods are sensitive to almost all colours within the visible light spectrum.
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Thus, Rods are very good at sensing white light, which is made up of the entire visible light range. On the other hand, this lack of specificity means that Rods can not sense different colours as they can not distinguish between different wavelengths. Sensing colour is achieved by the second type of photoreceptors; Cones…

Slide 6: Photoreceptors: Cones
Humans have three different types of cones, each with a distinct type of opsin sensitive to different ranges of wavelengths.
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The short cones respond to wavelengths in the blue end of the spectrum (CLICK), so are also referred to as blue cones.
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The medium cones respond to an overlapping but slightly longer range in the green portion of the visible spectrum,
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so they’re also called green cones. Lastly,
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the long cones respond to longer wavelengths in the red end of the spectrum
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so as you can guess are also referred to as red cones.
Unlike rods, cones collectively convey information about colour. The colours we perceive depend on which types of cones respond and how much signal each sends to their targets.

Slide 7: Phototransduction: Retina – Brain
So as light enters through the eye
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it makes its way to the back layer of the retina
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reaching the discs in the outer part of the photoreceptors
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When the light reaches the photoreceptors it causes a conformational change in the light-sensitive rhodopsin molecules
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which in turn alters ion movement across the membrane initiating the release of neurotransmitters from the photoreceptor cells.
Once photoreceptors transduce light photons into electrochemical signals, they begin the process of transmitting visual information towards the visual cortex and other parts of the brain.
This process begins by photoreceptors releasing neurotransmitter at synapses located at their terminals.
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Photoreceptors synapse with two distinct types of neurons – bipolar cells
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and horizontal cells
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The horizontal cells modulate the signal that is passed from the photoreceptors to the bipolar cells, which in turn pass the message on to the next layer in the retina. After the bipolar cells, the signal is sent to the next synaptic junction
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which involves two other cell types, the retinal ganglion cells
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and the amacrine cells.
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The amacrine cells, like the horizontal cells, modulate the activity in a sideways direction so it grooms the communication between the bipolar cells and ganglion cells. Finally, the axons of the ganglion cells, which make up the optic nerve
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carry the signal away from the retina and towards the brain.
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Therefore, the flow of neuronal information runs in this direction from the back of the retina to the front and then out of the eye via the optic nerve.

Slide 8: Visual Transduction
Taken together, the retina is one of our most vital sensory transduction sites. Light is funnelled and focused through the front of the eye to the retina. Once at the retina, specialized photoreceptors convert light signals in electrochemical signals that can be used and processed by the nervous system.

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Tricky Topic: Binocular Depth Perception

Slide 1: Binocular Depth Perception
The ability to discriminate between what’s near and what’s far is known as depth perception. Depth Perception relies on two types of cues – monocular and binocular. Monocular cues allow us to judge depth with the use of one eye, but binocular cues require the use of BOTH eyes.
This tricky topic will focus on binocular depth cues.

Slide 2: 3D World from 2D Images
We can easily perceive height, width, and depth in our 3-dimensional world, but it may surprise you that the images that are projected onto the retina are only in two dimensions:
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height and width. So how are we able to perceive depth??
The biggest influence on our ability to perceive depth comes from binocular depth cues. That is information coming from both eyes,
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which provides depth information to the brain.
To better visualize how images from the visual world travel from the eyes to the brain, let’s look at a top-down view of the human visual pathway…

Slide 3: Visual Pathway
Information from our visual world enters both eyes, hitting each retina at a slightly different angle, so each eye gets a slightly different perspective of the visual scene.
We can divide our field of view into two parts: the left visual field and the right visual field. Light from the left visual field
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enters the inside part, contacting the retina, of the left eye
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and the outside part of the right
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After leaving the retina, the information from the left visual field then travels to the optic chiasm
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where the information from the LEFT eye crosses over to the right hemisphere while the information from the RIGHT eye REMAINS on the right side of the brain. The result is that all the information from the left visual field, which is picked up by both eyes, is in the right hemisphere
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The signal then travels to the thalamus
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and then finally to the visual cortex in the occipital lobe
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Similarly, the same sequence of events occurs for information from the right visual field
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which also travels to BOTH eyes,
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with the signal from the right eye crossing over at the optic chiasm
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so that all the information from the right visual field is in the left cortex
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which can then travel to the left thalamus
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and the left visual cortex in the occipital lobe
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Now that we understand how information from the visual fields enter the eyes, let’s look at some visual stimuli to try and see how those two images (the one projected on the left eye and the one projected on the right eye) differ.

Slide 4: No Title (Image of mug)
Let’s say you’re looking at this coffee cup with both of your eyes open, it would look something like this.
If you close your right eye and keep your left eye open
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the view of the cup changes. The shift happens in the opposite direction when you close your left eye and open your right.
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Keep switching between your left and right eyes
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and you will see each views the cup at a slightly different angle. This means that a slightly different image is being projected on to your right and left retinas.
You can try this yourself by holding your finger out in front of your face…

Slide 5: No Title (Image of Pointer Finger – Binocular Disparity Title Appears as Animation)
As you open and close each eye
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you’ll notice that not only does the view of your finger change, but so does the background – it also appears to shift.
Now, if you move your finger further away from your eyes
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and alternate between your left and your right eye open
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– what you should notice is that your finger, relative to the background, seems to shift LESS.
Your brain integrates the images from each eye, compares the relative differences between the two, and is able to interpret how far the item you’re viewing is from your face. The more of a shift, the closer the object, the less of a shift, the further away the object must be.
This phenomenon, known as BINOCULAR DISPARITY,
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is what movie producers use to trick your brain into perceiving 3 dimensions when you are watching 3D movies. The glasses you wear allow your eyes to perceive two slightly different images which your brain integrates into one 3-dimensional image.
In addition to binocular disparity, your brain is also able to use the information from the muscles that allow your eyes to move around in their sockets… Put your finger in front of you at about arm’s length. Now stare at your finger while moving it closer to your face…
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Slide 6: No Title (Image of Eyes)
As you move your finger towards your face, your eyes turn inward towards your nose to follow the path of your finger
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If you move your finger away again, your eyes turn away from your nose
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When your eyes move inward, this is known as CONVERGENCE.
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As your eyes converge, the muscles controlling the movement, contract. Your brain interprets this contraction and uses it to perceive distance.

Slide 7: Summary
So, to summarize, there are two binocular processes that contribute to depth perception.
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The first is, Binocular disparity, which is the comparison of the differences between left and right retinal images. Binocular disparity
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is useful for judging depth in the distance, beyond about 3m. The second process that contributes to depth perception is, Convergence,
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which is the feedback from contraction of the eye muscles,
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this is best for judging the distances of objects within about 3m of the face.

Slide 8: Binocular Depth Perception
Binocular depth perception comes in two flavours, but what they have in common is that these two methods require the use of both eyes. Our ability to judge visual depth is critical for us to gauge the distances between objects, and thus, to maneuver with ease through our 3 dimensional worlds.

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Tricky Topic: Auditory Transduction

Slide 1: Auditory Transduction
Hearing plays a vital role in how we interact with and navigate through our environments. Yet, how is it that we are able to detect and then transduce mechanical sound waves into electrochemical neural signals? As we’ll soon see, it is the remarkable organization and complexity of the ear, which enables auditory transduction.

Slide 2: The Ear
The ear serves as the sensing and transducing organ of hearing. Let’s begin by looking at the general organization of the ear. The ear consists of three anatomically and functionally distinct divisions:
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the outer ear; the middle ear; and the inner ear.
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The outer ear
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is on the outside of our heads. It’s the part of ear we can see. There are two main parts of the outer ear. The first part, the Pinna
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funnels sound waves
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into the second part, the auditory canal
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which then further funnels sound waves
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to the tympanic membrane (also known as the eardrum).
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The tympanic membrane is the division point between the outer and middle ear. When sound waves contact the tympanic membrane it vibrates at a rate proportional to the properties of those sound waves.
The middle ear
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is located on the other side of the tympanic membrane. It is an air-filled chamber consisting of three distinct bones (also called ossicles)
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which are connected to each other in series: The malleus (also known as the hammer)
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the incus (also known as the anvil)
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and the stapes (also known as the stirrup).
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This chain of ossicles links the tympanic membrane and the oval window.
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When sound waves hit the tympanic membrane, they are then amplified by the middle ear on their way to the oval window,
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thus, the middle ear serves as a signal amplifier.
Lastly, the oval window is the passage into the inner ear.
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The major structure we’ll focus on in the inner ear is the cochlea.
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The cochlea consists of spiralling fluid-filled tubes and can be recognized by its characteristic snail-shell appearance. It is here where the transduction of sound waves into neural signals takes place. Specifically, this involves the conversion of mechanical stimuli into electrochemical signals, which then signal further to the brain via the auditory nerve.
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To understand transduction, we must focus deeper into the structure of the cochlea.

Slide 3: Cochlea
If we take a closer look at the cochlea, we see that just past the oval window, there are fluid filled membranous tubes that wrap around one another in a spiral. If we take a cross-section of a tube in that spiral
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we will be able to look inside
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Lets further focus in on the middle canal, also known as the cochlear duct
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which runs the length of the coiled-up cochlea. If we zoom in even further
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we can see first, the basilar membrane
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which lines the bottom of the cochlear duct. Next, you may notice there is a group of cells embedded within the basilar membrane. The major cell type we’ll focus on here, the Hair cells
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which are sensory receptor cells. These are specialized cells that are able to respond to outside stimuli and synapse with sensory neurons. Hair Cells don’t look like “typical” neurons. However, changes in their membrane permeability, just as in neurons, leads to the release of neurotransmitters and graded potentials in the post-synaptic sensory neurons they synapse onto. The mechano-sensing ability of hair cells comes from the small protrusions on their top surfaces, called cilia
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These hair-like cilia structures are then directly attached to the tectorial membrane
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which is located in the middle of cochlear duct. Taken together, the basilar membrane, the embedded hair cells and their cilia, and the tectorial membrane enable auditory transduction.
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When sound waves reach the inner ear, they initiate vibrations of the oval window, which then produces waves that travel through the fluid filled cochlear duct. You can image ocean waves closing in on shore or a wave pool where the wave generating engine is the oval window. As the wave is passing through the cochlear canal it initiates movements in the basilar membrane. The Basilar membrane is fairly flexible
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so it is able to move in response to wave propagation. On the other hand, the tectorial membrane is stiff
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and therefore is not able to move in response to wave propagation. Thus, in the presence of sound waves
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the basilar membrane moves up and down under the stationary tectorial membrane. Remember, the basilar and tectorial membranes are connected by the hair cell cilia, thus, as the basilar membrane moves up and down it causes bending of the hair cell cilia
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When the cilia bend, mechanosensitive channels open inducing electrochemical signals in the hair cells
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allowing for neurotransmitter release onto auditory sensory cells, which then signal via the auditory nerve
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to the brain.

Slide 4: Auditory Transduction
Taken together, the outer, middle and inner compartments of the ear allow for the amplification and transduction of the sound waves that travel through our auditory worlds into usable neural signals, which eventually travel to our brains to be perceived and interpreted.

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Tricky Topic: Auditory Discrimination

Slide 1: Auditory Discrimination
Beyond detecting sound, how it is that we can detect different types of sound? How are we able to distinguish between the vast collection of sound waves we encounter throughout our lives?

Slide 2: Different Sounds?
What allows us to distinguish between a pop song on the radio, and say, our smoke detector alarm? At least in part, the answer lies in the cochlea. But before getting into how the cochlea achieves the discrimination of different sounds, lets briefly review the properties of sound waves.

Slide 3: Properties of Sound
For now, we’ll focus on two of the major properties of sound: Frequency and Amplitude. Frequency, measured in Hz,
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refers to the number of wave cycles per second. For example, here we can see a low frequency wave
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and a high frequency wave.
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The frequency of the sound wave determines its pitch
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or tone. So, a low frequency sound wave would be a low pitch. Think about the beating of large drum.
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In contrast, this high frequency wave would be a high pitch. Think about a referee blowing a whistle.
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The second property we’ll look at is Amplitude
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which is a measurement of the intensity or the volume of a sound wave. The amplitude is a measure of the height of the wave. Two sounds of the same pitch can have different amplitudes. For example, this wave
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has a small amplitude and would be a soft sound.
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While this wave has a large amplitude
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and would be a loud sound
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So, now that we know sound waves come in different forms, how does the cochlea distinguish between different types of sound waves?

Slide 4: Coding Pitch
Let’s first focus on how the cochlea identifies pitch. Several theories have been proposed for pitch perception. Here, we’ll focus in on the two main theories of pitch perception: the temporal theory and the place theory. First, the temporal theory
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states that Hair cells bend at a rate proportionate to the sound wave frequency
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and thus auditory neurons will fire action potentials phase locked with the frequency of the sound wave.
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However, there is a physiological limit to how quickly action potentials can be generated due to the absolute refractory period. This limit is approximately 1000 HZ. This presents a problem, as Humans can hear from 20 – 20000 HZ.
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Thus, phase locking only enables for a small range of frequencies that humans can hear.
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So, what mechanisms enables the sensing of wavelengths with frequencies greater than 1000 Hz?
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This is where the second theory comes in; place theory.
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Sound waves entering the cochlea will reach a peak in basilar membrane movement at different distances from the oval window. This distance is dependent on the frequency of the sound wave.
This is because the properties of basilar membrane vary along its length
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Closer to the oval window
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the basilar membrane is much more narrow and stiff
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while further away from the oval window, near the centre of the cochlear spiral, the basilar membrane is wider and more flexible
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These different properties of the basilar membrane determine how different locations of the basilar membrane react to different sound wave frequencies.
High frequency sound waves peak near the oval window.
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Low frequency sound waves will peak furthest away from oval window at the centre of the cochlea spiral.
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And medium frequency sound waves peak closer to the middle of cochlea.
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Thus, the cochlea can discriminate between different sound wave frequencies depending on where they induce peak movement in the basilar membrane.
Now that we’ve looked at pitch, what about amplitude?

Slide 5: Amplitude
Sound wave amplitude is coded by the extent of movement of the basilar membrane. The larger the amplitude of the sound wave
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the larger the displacement of the basilar membrane, and therefore, the more the hair cell cilia will bend
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With greater bending of the cilia, more mechanosensitive receptors will be activated, thus initiating larger electric signals, more neurotransmitter release, and more Action potentials in the auditory nerve
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traveling to the brain.

Slide 6: Auditory Discrimination
Not only is the cochlea able to sense sound waves, but it is able to distinguish between specific properties of sound, such as pitch and amplitude. This information then travels along the auditory nerve to the brain where it can be further processed and perceived.

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Tricky Topic: Measuring Consciousness

Slide 1: Measuring Consciousness
This topic is tricky for a number of reasons. First, it’s not easy to define consciousness, which makes it difficult to measure. Second, if we do take the plunge and define a concept as abstract as consciousness, we place boundaries around what is included and excluded. The public looks to science to settle issues about consciousness in order to address ethical questions such as determining the end of life. Critical evaluation of the evidence used to make these important distinctions requires information about the strengths and limitations of the methods used by psychologists, neuroscientists use to study consciousness. For this tricky topic I’d like you to take a moment to consider the broader implications of measuring consciousness.

Slide 2: Why Does This Matter?
Let’s consider some famous cases. In 1995, Jean-Dominique Bauby, was almost completely paralyzed after a stroke. However, he had complete awareness of his surroundings and is shown here communicating by blinking his left eye. It was by this tedious method that he was able to write a book about his experiences, The Diving Bell & the Butterfly. Bauby died days after the publication of his book in 1997.
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Another famous medical case of abnormal consciousness was highlighted by the life and death of American Terri Schiavo. Schiavo lived the last 15 years of her life in a persistent vegetative state, and her subsequent death in 2005 by removal of her feeding tube divided not just her family but also the opinions of a nation. Former Israeli prime minister Ariel Sharon
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was in a permanent vegetative state for 8 years following a stroke and died following health complications from kidney failure in January of 2014. Although he was most certainly alive, his non-responsiveness led the Israeli Cabinet to declare him permanently incapacitated and unable to rule. Defining consciousness is not just a scientific question, but also a legal and moral one since it is considered to be a key component to a full life.

Slide 3: Defining Consciousness
A perfect definition of consciousness does not exist, but for the purposes of this lesson we will use a working definition. Most theorists would agree that consciousness involves awareness of one’s surroundings as well as the contents of one’s mind. This type of awareness is key for a lot of the things our brains allow us to do, such as to feel, see, hear, and remember, but is also the cornerstone of the uniquely private experience of just being who we are. How do psychologists and neuroscientists objectively measure such a subjective state. Typically it involves assessing how awake and aware an individual is.

Slide 4: Two Dimensions of Consciousness
Psychologists and neuroscientists focus on two dimensions of consciousness in attempting to identify conscious states. Wakefulness represented along the bottom of this figure
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refers to degree of alertness, and distinguishes waking from sleeping.
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Awareness refers to the degree to which we monitor our outer and inner environments.
According to this view of consciousness, each dimension ranges from low to high and all states of consciousness exist somewhere within this two dimensional space. So for instance, coma represented in the bottom left of this graph here
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is characterized by low wakefulness and low awareness whereas conscious wakefulness in the top right
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is characterized by high wakefulness and high awareness. Lucid dreaming,
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happens when someone is having a dream and are fully aware, so this unusual state is characterized by low wakefulness (since the dreamer is sleeping) but high awareness. Although this model is not perfect, as we’ll see shortly, it does help to point out some important components of consciousness. Let’s take the low end of both dimensions of this 2 dimensional view.

Slide 5: Measuring Minimal Consciousness
Coma patients have very low awareness and wakefulness, but there are a range of mental states that could be considered comatose. The Glasgow Coma Scale developed by two neurology professors at the University of Glasgow’s Institute of Neurological Sciences, is the most widely tool to measure consciousness in medicine. It uses three particular behaviours, eye opening, verbal response, and motor responses. This scale classifies patients as mild (score ≥ 13), moderate (8-12), or severe (< 8). Someone with a score of 3 would basically have no observable activity at all. In a vegetative state, one form of minimal consciousness, an individual is clearly awake, but does not appear to have much awareness, which appeared to have been the case with Terri Schaivo. On the other hand are individuals with locked-in syndrome, like Jean-Dominique Bauby who, though fully conscious, had very little control over his own voluntary movements. These cases of paralysis with intact cognition pose a significant challenge in medicine because it is difficult to determine the level of consciousness using the Glasgow Coma Scale.

Slide 6: Imaging the Conscious Brain
Conditions such as locked in syndrome have prompted efforts to find new ways to assess the level of conscious in patients with traumatic head injuries. Some recent findings using neuroimaging techniques have shown promise. In 2006 researchers at the University of Cambridge found evidence of consciousness in a patient in a vegetative state. Using functional MRI,
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researchers found that her auditory areas in her temporal lobe
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were active when listening to speech.
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Furthermore, when asked to imagine certain actions, such as playing tennis or walking around her home, she showed the same brain activation as a control patient without head injury. The fact that she could respond with her own brain activity in an intentional, purposeful way allowed her to communicate despite her inability to make motor responses. Other neuroimaging techniques are based on EEG, which is measured from electrodes placed on the head.
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This technique has revealed that some patients undergo predictable changes in brain activity
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seen over a typical night’s sleep. Event-related potentials,
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or ERPS, are particular patterns of EEG waves that signify brain reactions to particular stimuli or events. ERPs have been used to evaluate complex functions such as attention, memory, and language which makes this well-suited to assessing aspects of consciousness. The Halifax Consciousness Scanner is an EEG-based system developed by mindful scientific that uses a customized headset to record brain responses. What all of these imaging techniques have in common is that they measure brain responses, rather than behaviours, and therefore can be used in patients with little to no motor control.
So far we have considered consciousness as having high and low levels, and that we can move up and down these levels.

Slide 7: Measuring Full Consciousness
What about when we are fully awake or aware? Are we “maxed out” during full consciousness? One view is that consciousness shifts to events or tasks that are most relevant. In other words, our conscious processes latch onto what happens to be meaningful to us at a particular moment. In other words, rather than asking how much consciousness someone is displaying, this perspective focuses on where conscious efforts are being spent. A lot of what we do in our everyday lives requires our conscious effort and attention, such as reading a chapter in a textbook. However, an awful lot of what we do happens beneath our level of awareness. Take the act of reading itself. Once learned as a child, our consciousness about the process of reading is no longer required so it happens automatically. In fact, once learned, it is difficult NOT to do (just try looking at the words on the screen WITHOUT reading them). The involvement of consciousness in our everyday lives is illustrated by an experiment by researchers at the UWO using the Ebbinghaus Illusion, shown here.
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Although the central circle on the left
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is the same size as the one on the right
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the one on the left appears larger. Our conscious visual perception produces the illusion of two differently sized objects. An interesting disconnect happened when the researchers asked participants to grasp the central circle. When grasping either central circle, participants held their fingers the SAME distance apart, indicating that motor responses are not fooled by the conscious visual illusion.
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Another example of the divided nature of consciousness comes from studies of attention. Selective attention is the ability to focus awareness on specific features in the environment while ignoring others. Ignoring unnecessary or irrelevant information is important, but it means that we often miss things. In this picture,
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participants had a difficult time noticing the person dressed in the gorilla suit if they were asked to keep track of people wearing white t-shirts. Selective attention can result in inattentional blindness or change blindness, whereby we miss things because we are selectively attending to something else.

Slide 8: Can We Measure Full Consciousness?
So can we measure full consciousness? Because full consciousness is not packaged neatly into levels, it may seem impossible.
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However, we can become aware of conditions when our consciousness shifts. For instance, imagine that you are at a crowded party
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having a conversation with a couple of friends. The background noise is largely ignored because you direct your attention to the conversation. However, if someone in the crowd says your name, your attention shifts to the background noise that you had previously blocked out. This ability to filter out sounds and then refocus attention when you hear your name is called the cocktail party effect. Tuning out information is not always a good thing,
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particularly when driving. Most Canadian provinces have banned the use of hand-held devices while driving, however the practice of talking and texting while driving is still widespread. Research has shown that talking on a phone while driving produces gaps in attention and perception, even while using a hands-free phone.
So although it might be difficult to directly measure full consciousness in the way that we measure coma states, we can certainly examine conditions under which full consciousness is interrupted.

Slide 9: Measuring Consciousness
Measuring consciousness is not straightforward, but understanding what we CAN measure helps us appreciate what types of questions we can ask.

To be updated to reflect new video at a later date

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Tricky Topic: Rhythmic Nature of Sleep

Slide 1: The Rhythmic Nature of Sleep
As I’m sure you’ve noticed, your level of consciousness varies through daily waves of sleep and wakefulness. This rhythm is so predictable that we humans plan all of our activities to fit into this cycle. Although people differ in their sleep habits, since some people are early risers and others are night owls, everyone’s sleep and activity patterns fit into the context the daily cycle of day and night.

Slide 2: Circadian Rhythms
In fact, all sorts of biological and psychological processes follow this daily, or circadian, rhythm,
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from the Latin for circa, meaning about or approximately and dian, meaning day. This figure,
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shows the typical, daily temperature rhythm for a human. The darker shaded blue region indicates night,
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when daily temperature starts to dip. With the return of the sun the next morning,
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body temperature starts to rise again, and the cycle repeats itself every day. Many hormones also follow daily patterns of rise and fall, this here
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shows the daily rhythm of melatonin, a hormone that promotes sleep. Its pattern is opposite to that of daily temperature; it rises just around the time we go to sleep and drops to very low levels during the day. Not surprisingly,
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self-reports of alertness also vary throughout the day, with highest alertness during the daytime and lowest levels in the middle of the night.
Although these rhythms appear to follow the external light-dark cycle, they are not slaves to the schedule of the sun. In fact, these rhythms are generated internally by a small collection of neurons in the brain.

Slide 3: Free-running Rhythms
When people live under conditions without the regular appearance of dawn and dusk, their temperature, hormone, activity, and sleep rhythms follow a pattern that is close to, but not exactly, 24 hours. These are called free-running rhythms and are ENDOGENOUS,
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meaning that they’re internally generated by specialized areas of the brain. They’ve been extensively studied in hamsters
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living in constant dim light. Hamsters love to run on their wheels when they first wake up, and because they are so dedicated, the beginning of their day’s running is an excellent way to track these free-running rhythms. But how can we test free-running rhythms in humans? Most people wouldn’t want to live in an environment without time cues, but several people volunteered to live for a period of months in underground bunkers
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as part of a research study. They woke up a little later every day and eventually their rhythms were disconnected from the day and night cycle. Results from this and similar studies reveal an endogenous rhythm of a close to 25 hours in humans. Free-running rhythms have also been documented in natural conditions of constant light or dark, such as in the Arctic, and in certain types of blindness.
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The reason that we don’t free run is because our rhythms are reset each day by light, ensuring that our internally generated rhythms are synchronized to our environment. Shortening or lengthening our days by traveling across time zones
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or working shifts throws off this synchronization, and it takes time for the body to readjust to the new daily cycle.

Slide 4: Ultradian Rhythms
The last type of biological rhythm we’ll consider are ultradian rhythms, that repeat on a cycle less than 24 hours. One example of an ultradian rhythm is the sleep cycle,
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when the brain and body undergo a pattern of changes about every 90 minutes. Some of this activity can be observed by simply watching someone sleep. Rapid eye movement, or REM, where the eyes move around underneath the eyelids
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occurs in bursts throughout a night’s sleep. The amount of REM changes throughout the night
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but the frequency is fairly consistent, kicking in every 90 minutes. Other changes that occur during sleep, like dreams
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are not easy observed by watching from the outside, but we’ve all experienced weird and wonderful adventures inside our own heads when we sleep. Studies show that people are more likely to report dreams if they are woken up during an episode of REM than non-rapid eye movement sleep
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so REM sleep has a special relationship with dreaming
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Non-REM sleep
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is divided into four separate stages based upon the depth of sleep
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Sleep depth can be measured by determining how hard it is to wake someone up. Researchers do this by using the acoustic arousal threshold, which is a fancy term for the amount of sound required to for awakening (EXAMPLE: *whisper* “Hey Michael, wake up.” compared to *SHOUT* “HEY MICHEAL, WAKE UP!”). Stage 4 is the deepest level of sleep because it has the highest acoustic arousal thresholds.
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REM sleep usually follows Stage 4 sleep, but in many ways, it’s more similar to waking. This is most obvious by comparing patterns of brain activity during the different stages.

Slide 5: EEG Rhythms During Sleep
For many years, it was assumed that the brain was fairly inactive during sleep. Since a major feature of sleep is a dramatic reduction in movement, early psychologists had few tools to study sleep. With EEG technology,
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scientists have learned that brain undergoes predictable changes with shifts in wakefulness and awareness.
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This shows brain activity for someone who went from a state of relaxed drowsiness, represented by the higher frequency alpha waves to the left of the arrow, to a light sleep, shown by the appearance of theta waves to the right of the arrow. Interestingly, alpha waves occur during REM sleep, but not during non-REM sleep stages. As levels of wakefulness change during non-REM, so do these brainwaves
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and has allowed sleep to be roughly divided into these four stages of non-REM sleep. Stage 2 EEG somewhat resembles stage 1 whereas stages 3 and 4 show a lot of delta waves, large slow waves like these here.
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Since these stages of sleep have a large amount of these slow delta waves, they are often called slow wave sleep. Slow wave sleep is the deepest level of sleep, since that’s when we’re least responsive to the outside world.

Slide 6: Sleep Over the Lifespan
As this graph shows, infants and young children, shown on the left,
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sleep more than older children and adults. Not only is the amount of sleep greater, but they also spend significantly more time in REM sleep. During adolescence and adulthood, the amount of sleep that involves REM steadily decreases. The high degree REM during the beginning of life has led some to suggest that REM sleep might be important for supporting brain growth and development.

Slide 7: The Rhythmic Nature of Sleep
So hopefully you can appreciate the complicated nature of this strange activity that we engage in every single night.

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Tricky Topic: Hypnosis

Slide 1: Hypnosis
Hypnosis is one of the most fascinating topics in the study of consciousness, and at times the most controversial. This tricky topic will outline different theories and research on this mysterious state of mind.

Slide 2: Hypnosis Defined
Hypnosis is tricky to define, since not everybody agrees on its characteristics. However, most would agree that it’s a state of consciousness with extreme self focus and
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minimal attention to external stimuli.
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Under some circumstances hypnosis increases suggestibility,
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and (sometimes) suspension of critical thinking.
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Usually some sort of method is used to induce a hypnotic state,
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which typically involves fixating the eyes on a single object or area and having the person relax. It’s important to make a distinction between different types of hypnosis.

Slide 3: Stage Hypnosis
Stage hypnosis is the entertainment side of this business, but is this real hypnosis? Is the volunteer showing focused attention, suggestibility, lack of voluntary control, and suspension of critical thinking? If so, is this a special state of consciousness induced by the hypnotist, or is the apparently hypnotized person just playing along so as not to disappoint the large audience expecting to see a good show? Keep in mind that the subjects of the stage hypnotist are audience volunteers,
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who might be more obedient and compliant compared the majority of people who are sitting in their seats. What they see
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is the hypnotist inducing a trance-like state, and the volunteers obey any command. As a quick search of YouTube will show you, stage hypnotists command volunteers to engage in all sorts of silly acts such as dancing with an imaginary partner or barking like a dog. This ability to control others would make hypnotists incredibly powerful in the real world, sort of like a superhero wizard,
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so it seems unlikely that anyone is really that powerful.

Slide 4: Hypnotherapy
Stage hypnosis should not be confused with hypnotherapy, which uses hypnosis to achieve therapeutic changes in thoughts, feelings, and behaviour. This emerged prominently in medicine during Victorian times, when it was used to treat a variety of disorders,
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in fact, Freud used it to tap into the unconscious mind.
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Modern applications of hypnosis include treating pain during childbirth, dental procedures,
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and surgery.
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Furthermore, there has been some promise in the use of hypnosis for quitting smoking
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and reducing nausea associated with many cancer therapies as well as anxiety.

Slide 5: How? Two Perspectives
There are two broad perspectives on hypnosis.
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One explanation, suggested by Ernest Hilgard, is that hypnosis is a special state where there’s a dissociation of the conscious mind from events happening during hypnosis. Hilgard described this as the hidden observer effect
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after he demonstrated that one aspect of a person’s mind can remain aware of stimulation from the outside (such as the hypnotist’s voice), while other parts of the mind are cut off from external input. To demonstrate this, Hilgard hypnotized a man and told him he was deaf. While in the hypnotic state, the man did not respond to sudden, loud noises nearby, which most of us do instinctively. Next, Hilgard told the man to raise a finger if he could hear him and the man immediately obeyed.
An alternative view,
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supported by Martin Orne and Nicholas Spanos, is that hypnotized people behave as they are expected, according to the social context and expectations, so they essentially play a role under hypnosis. Martin Orne’s research revealed that most participants in psychological experiments are incredibly obedient, and would do tedious tasks (such as completing endless pages of math problems and then ripping them up) or even downright dangerous ones (such as picking up a snake they believe is poisonous). So this perspective suggests that obedience under hypnosis is not a special phenomenon, and does not require a special state. Needless to say, both sides of this debate argue with each other.
What they can both agree on, however, is that hypnosis has powerful effects on thought, emotion, and behaviour. So you might wonder, what’s happening in the hypnotized brain?
One common approach to studying the brain during different states of consciousness is to use neuroimaging, such as fMRI.

Slide 6: Neuroscience of Hypnosis
In one experiment, researchers used a Stroop task to examine how the brain responds to hypnotic suggestion.
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The Stroop looks at the delay in reaction time with conflicting information, by measuring the difference in how long it takes to name the colour of text when the meaning of the word matches, compared to when it doesn’t match. It sounds confusing but is easily illustrated with an example. As fast as you can, name the colour of the text for these three words, ready?
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Now name the colour of the text for these three words, ready?
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The 2nd set of words is more difficult because we automatically read the word instead of focusing on the colour of the print, so it usually takes people longer. Before the task, the researchers hypnotized people
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and introduced a post-hypnotic suggestion: when they hear a certain voice, the words in the Stroop task are gibberish
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and completely incomprehensible, and on other trials they’ll see actual words. In fact, none of the words were gibberish but they found that easily hypnotizable participants
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did not show a Stroop effect when they thought they were viewing gibberish words, while the less hypnotizable participants still showed the slowing of reaction time for the difficult condition.
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Hypnotizable people showed faster colour naming
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even when the words and colour were mismatched. Furthermore, they showed LESS activity
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in the areas of the brain that deal with conflicting information.
Since the Stroop task is performance-based, it’s hard to fake it, which argues against the role playing hypothesis. The fact that brain imaging showed reduced activity in certain areas suggests that the hypnotizable people are actually dissociating two brain processes, providing some support for the special state hypothesis.

Slide 7: Pain in the Brain
Another study, by Derbyshire and colleagues at the University of Birmingham, looked at the effect of hypnosis on pain perception, which is known to be strongly influenced by psychological factors.
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They recruited highly hypnotizable people and had them rate pain on the hand
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in one of three conditions:
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real physical pain by touching the hand with a hot metal probe,
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imagined pain,
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and pain induced by hypnosis. Mind you, it was not induced by a wizard, but one of the researchers.
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They measured two responses: self-rating of pain and brain activity. What they found was that the self-reported pain ratings
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were highest for real physical pain
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followed by hypnotic pain while those who imagined pain did not report any REAL pain at all.
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Also, the pattern of brain activity was almost identical for real and hypnotic pain, compared to imagined pain.

Slide 8: Summary
So what can we take from this? In summary,
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it’s clear that hypnosis has powerful effects.
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There is some evidence for the special state hypothesis, both in studies of cognition with the Stroop task as well as pain perception.
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Brain imaging shows that the brains of hypnotizable people sometimes respond differently (in terms of the Stroop task) or similarly (in terms of pain) compared to controls, so the effect of hypnosis is far from straightforward.
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One final word of caution: these studies described all used participants who were easily hypnotised, and therefore these findings might not apply to everybody.

Slide 9: Hypnosis
Although there no clear consensus on how hypnosis works, for some people at least, it can influence thought and behaviour in potentially therapeutic ways.

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Tricky Topic: Atkinson-Shiffrin Model of Memory

Slide 1: Memory: Atkinson-Shiffrin Model
How are memories formed, rehearsed, and retrieved? How do the aspects of memory interact with and complement one another? One model that has been proposed to answer these questions is the Atkinson-Shiffrin Model.

Slide 2: Atkinson-Shiffrin Model
Think about going for a nature walk. During that walk you are constantly receiving a stream of sensory input into your sensory memory.
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The Atkinson-Shiffrin Model for memory starts with all the sensory information from your environment being received and coming into your sensory memory.
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In order to retain information in your sensory memory, you need to pay attention to it. Thus, information is filtered and select from our sensory memory to our Short-Term Memory by our attention.
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Not to confuse yourself, Short-term memory is often interchangeably referred to as working memory. Information within your Sensory memory that you do not pay attention to is lost.
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Let’s come back to our nature walk. You would not remember every moment of the walk and all aspects of the trail you saw and heard. This is because the majority of the sensory input into your sensory memory is lost because you don’t pay attention to it. However, the specific sensory inputs you do pay attention to will be passed into your Short-term Memory. For example, let’s say you love flowers and you notice a beautiful yellow wildflower as you start your walk,
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this will then get passed into your short-term memory.
Once in your short term memory, information is further filtered and selected for depending on how much you rehearse, and thus, maintain that memory.
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Information at this point that is not rehearsed, will also be lost.
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Think again back to the nature walk. Imagine around your next turn you see an even more beautiful purple flower.
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Now, as you continue on your walk you are thinking of the more beautiful Purple flower and no longer about the yellow flower. Thus, you are rehearsing and maintaining the memory of the purple flower, while the memory of the yellow flower may be lost due to a lack or rehearsal.
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Finally, if information in your short-term working memory is ENCODED, then it can be stored in your long term memory.
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Once this information is stored, it may be retrieved and brought back into your short-term memory at a later time point.
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Again, back to your nature walk example, you likely will not continuously think about the purple flower for the rest of the day
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– it may leave your short-term memory – but later than evening if someone asked about your walk, you might easily retrieve the memory of the purple flower from your long-term memory.
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However, if you were asked about that walk in 10 years, it’s possible that you wouldn’t recall anything about the purple flower,
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or potentially even the walk! This is because some information is lost over time from your long-term memory.
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If we take a bit of a closer look at each of the three memory stages, we can see that each stage has a unique information capacity and retention duration.
First, sensory memory
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has a large capacity and a very short duration (usually seconds or less).
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Think about all stimuli coming in from the environment at any given time.
Second, short-term memory
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has both a small capacity as well as a relatively short duration.
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Remember, this is the memory stage that allows you to think about present sensory information and work on problems in the immediate moment. Working memory may last about 18-20 seconds.
Finally, Long-term memory
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has both a huge capacity and a very long duration.
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In fact, there are no known limits to long term memory and certain memories may last for the entirety of a person’s lifetime.

Slide 3: Memory: Atkinson-Shiffrin Model
The Atkinson-Shiffrin Model presents a way to interpret how our memories are formed, worked on, and later retrieved. While it is important to understand that this model is a working hypothesis, it provides a strong rubric for how we might interpret and better understand memory.

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Tricky Topic: Baddeley’s Model of Working Memory

Slide 1: Memory: Baddeley Model
Let’s consider working memory, which is often interchangeably referred to as short-term memory. This is the memory that actively works on information, where we think about and process things; it is a very active place.

Slide 2: Baddely Working Memory Model
Dr. Alan Baddeley, a memory researcher, proposed a way to think about how working memory functions. There are 4 key components to his model: the Phonological Loop, the Visuospatial sketch pad, the episodic buffer, and the central executive.
The first component we’ll focus on
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is the Phonological loop
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This is the auditory part of your working memory. It is what is being used when you’re saying things to yourself or listening to what someone else said over and over in your mind.
The next part is the visuo-spatial sketchpad
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This is the component of working memory that enables you to picture things in your mind and work on them. This is also how you are able to have mental maps of things – picture in your head the streets and locations of things.
The third component is the episodic buffer.
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This is the area of your working memory where you are temporarily storing information you’ve brought up from your long-term memory.
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Finally, there is the central executive
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– this is the part that is in control of everything. It decides how much attention to pay to each of the parts of working memory, brings info from long-term memory and puts things together.
Keep in mind that this is just a concept of how working memory works. There are no specific brain structures that are designated for these processes, although, the central executive is considered to be something fairly concrete and is thought to be mainly processes in the prefrontal cortex.
Let’s take a quick look at how this working memory model might apply to a real example. Let’s say you are asked to add 87 plus 36. As you are asked to perform this calculation your Phonological loop is hearing the numbers and then repeating them in your mind allowing you to remember then. Next, you may use your episodic buffer and visuospatial sketch pad to recall and then picture the addition strategy you learned back in grade school
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Finally, your central executive would integrate these three aspects of your working memory to solve the equation, 123

Slide 3: Memory: Baddeley Model
As working memories are in constant use, they require the integration of both new sensory inputs and old long-term memories. The Baddeley Working Memory model offers a hypothesis for how we are able to integrate these two information streams and solve problems moment to moment throughout our daily lives.

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Tricky Topic: Biological Basis of Memory

Slide 1: Biological Basis of Memory
We have many different types of memory, and in turn, many different brain areas that are involved in working together to allow us to interact and remember skills, events, our environment, and so on.
Let’s take a closer look at some of the areas of the brain associated with memory. As we will soon see, memory involves many areas of the brain working together.

Slide 2: Sensory Memory
The cerebral cortex
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is believed to be where the majority of sensory information is processed – that is what you are seeing, hearing, where you are, and what that information all means. As sensory information ascending to your brain it first is sent to the thalamus. From there, signals from different sensory modalities are sent to and processed by different areas of the cerebral cortex depending on the sense.
Vision is primarily processed in the occipital lobe
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Audition, as might make sense, is processed in the temporal lobe right next to the ears
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Touch is processed in the somatosensory cortex which lies in the parietal lobe
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Taste is processed in the frontal and temporal lobes
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And lastly, smell or olfaction, is processed in the olfactory bulbs, which are actually not apart of the cerebral cortex but lie just above the cribiform plate

Slide 3: Working Memory
It is important to note that different sensory modalities are constantly being processed at the same time in your working memory. As we just learned, all of these different processes are taking place in different parts of the brain. As such, distinct aspects of Working Memory Models can be hypothesized to be occurring in distinct cortices of the brain.
Let’s consider the Baddeley Working Memory Model.
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When you are picturing images in your mind, you’re engaging your visuospatial sketchpad, and you are using your occipital lobe
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Repeating things (or talking to yourself in your head), is the act of engaging the phonological loop, which activates parts of the cortex involved with hearing, speech, and language in the Frontal and Temporal lobes
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And then finally the central executive, that plans and organizes your thoughts, is localized in your prefrontal cortex

Slide 4: Memory Consolidation
If we move from sensory memory to working memory, and then finally to long-term memory, we must acknowledge the role of the mighty hippocampus, which sits inside the cerebral cortices. The hippocampus can be visualized in this 3D representation
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or by taking a sagittal section down the midline of the brain looking at it from a medial view.
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The act of consolidating memory, or moving memories from temporary to long-term storage, is carried out by the hippocampus.
Let’s look at a simple example of how the hippocampus interacts with the cortex in memory processing.
Let’s say visual Information,
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processes by the eye, is sent to the thalamus,
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then to the corresponding visual cortex in the occipital lobe.
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This visual information in the occipital lobe can be sent to the hippocampus for consolidation.
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Information can then be sent back from the hippocampus to the cortex for long-term storage.
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This is why, when we are experiencing something – for example, seeing someone’s face – our visual cortex is activated, but it’s also activated when we THINK about a person’s face in their absence.

Slide 5: Long-Term Memory
What about long-term memory? First, before exploring the brain structures associated with long term-memory we just should distinguish between the two general types of memory: Explicit memory and Implicit memory. Let’s begin with explicit memory,
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which refers to information about events and facts that you are conscious of. As we just saw, explicit memory is processed by the hippocampus and then sent for long-term storage in the cortical area that corresponds to the specific information type.
For example, Visual information is sent from the hippocampus after consolidation, to the visual cortex in the occipital lobe.
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Auditory information is sent from the hippocampus to the auditory cortex in the temporal lobe,
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somatosensory information is sent from the hippocampus to the somatosensory cortex in the parietal lobe,
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and so on.
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But, what about memories like how to ride a bicycle or tie your shoes or why you could drool every time you hear a bell ring?

Slide 6: Long-Term Memory (Implicit Memory)
Implicit memories, those memories for procedural things like playing a musical instrument, habits, and skills tend to be stored in structures below the cortex, known as the subcortex.
The striatum,
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which is part of the basal ganglia, is responsible for procedural memories like sport skills and physical habits.
Memories for precise movements like playing a musical instrument involve the cerebellum
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And finally, the amygdala
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is responsible for the associations we have between emotions and events, such as graduation! In fact, our amygdala is what is responsible for our tendency to remember emotional stimuli better than neutral stimuli.

Slide 7: Biological Basis of Memory
As it may now be clear, the formation, consolidation and retrieval of memories requires ongoing and dynamic processes of numerous structures throughout the brain. Hopefully by now you can appreciate the immense brain complexity underlying everything from your most precious to your most mundane memories.

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Tricky Topic: Classical Conditioning

Slide 1: Classical Conditioning
Classical conditioning, also called Pavlovian conditioning, after its founder Ivan Pavlov shown here, is the focus of this Tricky Topic.

Slide 2: Operant Conditioning Defined
Classical conditioning is one type of associative learning, where an individual makes a connection between two different stimuli or events. More specifically, classical conditioning occurs when a neutral stimulus becomes associated with a meaningful one, something that triggers an automatic response.
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So the types of behaviours involved in classical conditioning are involuntary responses, and psychologists often refer to these as “reflexive” behaviours.
What are some examples of reflexive behaviours? One is pain withdrawal. Say you happen upon this iron
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because you have to iron a shirt for a job interview later. Perhaps your roommate left it out for you, how considerate! You reach to grab it and discover it’s REALLY HOT, so you pull your hand away. That’s a reflexive behaviour in response to pain. The next time just the sight of an iron might automatically trigger an avoidance reaction because of your past experience.
Emotional responses are considered to be mainly involuntary, which is one of the reasons that emotions are often so difficult to control. For instance, if you hear a sudden loud noise,
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it will probably trigger an automatic startle response
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because it provokes fear. As you will learn in this tricky topic, sometimes it’s advantageous to know when something important is going to happen, so classical conditioning is all about attaching meaning,
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so that you can predict when things are going to happen, rather than passively responding to events in the environment.

Slide 3: Ivan Pavlov
You can’t get far in learning about classical conditioning without learning about Ivan Pavlov. He was a Russian physiologist who was awarded the Nobel Prize in Physiology or Medicine 1904, not for his work on associative learning, but for his research on saliva and digestion.
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He measured salivation in dogs when given different types of food, like meat powder. He noticed that, over time, the dogs would start drooling before they were given the meat powder, when the technician made noise assembling the equipment to measure their saliva.
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He hypothesized that the dogs made an association between the noise of preparing the equipment and the food that always followed. Rather than see this as a nuisance to his digestion research,
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he decided to investigate further and ask whether the dogs could learn to salivate to other sounds.

Slide 4: Pavlov’s Experiment: Before Conditioning
So this is what he did to test his hypothesis. Before conditioning, he found that the dogs would drool in response to meat, of course, because dogs find meat delicious. This is referred to as the unconditioned stimulus, called the US
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and the dog’s response is called the unconditioned response, or UR.
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These are both referred to as unconditioned because this response is reflexive, or unlearned. Before conditioning, a neutral stimulus, such as a non-delicious bell,
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does not produce salivation.
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He did all that in the beginning to make sure that dogs don’t respond to bells with drooling (this is an example of careful science.

Slide 5: Pavlov’s Experiment: During Conditioning
During conditioning, the neutral stimulus,
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is presented just before the US,
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and as expected, the dog salivates,
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just as it did when the US was presented alone. If this pairing is repeated enough times,
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Slide 6: Pavlov’s Experiment: After Conditioning
…then the dog now salivates upon hearing the bell, so this has now become a conditioned stimulus, or CS
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and the dog’s response to this new learned cue is called the conditioned response (CR)

Slide 7: Two Fundamental Rules
Through many, many careful experiments, Pavlov and his research group worked out two fundamental rules of classical conditioning.
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First, multiple pairings of the US (or natural stimulus) and the CS (or neutral stimulus) are necessary in order for the CS to take on the association.
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Second, the CS and US must be presented close together in time, and works best when the CS occurs just before the US, so it can act as a predictor.
Classical conditioning can change once it is established, in ways that can tell us something about what is going on in the mind of the learner.

Slide 8: Stimulus Generalization
For instance, stimulus generalization occurs when stimuli that are similar to the CS will also trigger the learned behaviour, even though these specific stimuli have NOT been previously paired with the US. It can reveal the types of things an individual finds similar. This is actually really handy in determining the sensory abilities of individuals who cannot speak, such as animals and babies.

Slide 9: Stimulus Discrimination
Stimulus discrimination training tells us what individuals consider different and it’s the first step in training animals. Dogs are trained to communicate with us about smells they are able to detect, like drugs and explosives. It’s an amazing collaboration. Without any fancy technology, using just treats, patience and knowledge of classical conditioning dogs are able to tell us about dangers that are invisible to us

Slide 10: Classical Conditioning in Action
An organization called Apopo has trained African giant pouched rats to clear huge area of Tanzania of landmines. They’ve been called HERO rats and this one shown here was specifically detect the smell of explosives. Their sense of smell is as good or even better than dogs, and because they’re smaller they’re unlikely to set off hidden landmines.

Slide 11: Extinction
Extinction is the disappearance of CR, when CS and US are no longer paired.
This happens when the CS appears repeatedly on its own,
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without the meaningful US,
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and the CR eventually stops happening.

Slide 12: Spontaneous Recovery
So the conditioned response doesn’t hang around forever when the CS is presented alone. This figure shows the strength of the CR on the y-axis, here,
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and what happens during training
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and during extinction
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when the CS is presented alone. When extinction is complete, it’s almost as if the learning never happened at all. However, Pavlov showed that if the CS is presented alone again after a delay the CR will spontaneously recover,
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although the size of the response is generally weaker. Therefore it’s likely that extinction suppresses learning but does not erase it.
Pavlov’s findings sparked all sorts of research on classical conditioning. American psychologist John Watson felt so strongly that he set out to test whether classical conditioning could be used to shape human behaviour.

Slide 13: Classical Conditioning in Real Life
In his now notorious study of Little Albert (1920), Watson and colleague Rosemary Raynor conditioned a baby to fear a tame lab rat by presenting it just before a sudden loud noise. Little Albert learned to fear the rat, as well as other fluffy white objects. This showed that his conditioned fear generalized to other stimuli. Little Albert did not undergo deconditioning so this research sparked a lot of ethical controversy. However, Watson showed that fear can be learned, and many successful treatments for anxiety problems such as phobias,
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are based upon unlearning conditioned fear responses.

Slide 14: Classical Conditioning
The knowledge of classical conditioning has revealed how our minds link events in a way to act as predictors

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Tricky Topic: Conditioned Taste Aversion

Slide 1: Conditioned Taste Aversion
Conditioned taste aversion is the rebel of classical conditioning, since it breaks some well-established rules. Let’s start with a real-life example.

Slide 2: Learned Food Aversions
For many people this pizza,
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probably triggers thoughts of yumminess but for other people, like Sherry, it provokes strong feelings of nausea.
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Why does Sherry feel this way about pizza? Many years ago, she had some pizza for lunch, and later on that day suffered from a nasty stomach bug and ended up spending the next 24 hours in the bathroom. Even though it wasn’t the pizza that caused this illness, she now has a life-long aversion to it, she hasn’t eaten pizza since. This experience is also common in people who’ve experienced gastrointestinal illness from food poisoning. This incredibly strong, LEARNED association between illness and food is known as conditioned taste aversion.

Slide 3: Conditioned Taste Aversion
Conditioned taste aversion is a learned avoidance of a particular taste, specifically when nausea occurs after food is eaten. If we compare what happened in Pavlov’s original experiments with Sherry’s learned aversion to pizza, we can see similarities.
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In both situations, there’s a stimulus that automatically triggers an involuntary response,
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meat makes dogs drool, and stomach bugs make us barf. In Pavlovian terms, these are the unconditioned stimuli
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and unconditioned responses.
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In both types of learning, there’s a stimulus that occurs before the US,
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which on their own shouldn’t trigger these responses. The PAIRING of these stimuli (the bell and the pizza) with the US results in them taking on new meaning, and they can then trigger the responses on their own.
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In Pavlovian terms, these newly learned triggers are called conditioned stimuli,
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and these learned reactions are called conditioned responses.
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Let’s take a moment to review Pavlov’s fundamental rules of classical conditioning.

Slide 4: Pavlov’s Fundamental Rules
First, multiple pairings of the CS with the US are necessary in order for the CS to take on the association.
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Second, the CS and US must be presented close together in time. These rules are based upon a mountain of laboratory research observed in meticulous experiments under tightly controlled lab conditions by Pavlov and others. However, Sherry’s conditioned taste aversion to pizza did not appear to require multiple pairings,
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in fact there was only one time when the pizza was paired with illness. Also,
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Sherry ate the pizza hours before the nausea set in. So conditioned taste aversion appears not to fit neatly with research on classical Pavlovian conditioning. Of course, Sherry’s learning happened in messy real life with a slice of pizza and a tummy bug, so it’s useful to look at this phenomenon in a laboratory setting. Conditioned taste aversion is also referred to as the Garcia effect, after John Garcia, whose classic research first investigated this.

Slide 5: John Garcia’s Research
Garcia accidentally stumbled upon his now famous research studying the effects of radiation exposure.
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He noticed that rats responded to low levels of radiation with reduced feeding as a result of gastrointestinal upset. Therefore he set out to ask two questions:
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Can rats be conditioned to avoid a sweet taste (which rats ordinarily love) if it’s paired with radiation, which makes them sick? And if so,
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how long does this food aversion last?

Slide 6: Garcia’s Experiment
So this is what he did to test his hypothesis. There were six groups of rats, exposed to one of three radiation conditions
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a no radiation control group, low radiation, and high radiation for a period of 6hr. For the 6hr irradiation period, rats were either given access to regular water,
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or water with the artificial sweetener saccharin.
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Keep in mind that there are two independent variables, 1) the level of radiation, indicated by the colours, and 2) the fluid they were given while exposed to the radiation, which is indicated on the water bottles. After this 6hr conditioning period, rats were given a choice between two drinking bottles, one with water and another with, you guessed it, saccharin water. The dependent variable was how much of the saccharin water the rats consumed. Like humans, rats like things that taste like sugar, so ordinarily they prefer sweet-tasting saccharin water over plain, unflavoured water. Since radiation produces gastrointestinal upset, Garcia hypothesized that the rats might associate their illness with the sweet taste and avoid it in the future.
And this is what he found.

Slide 7: Saccharin Preference
The main measure was the % of saccharin water the rats drank when given a choice,
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shown here on the y-axis on the left. Rats that got water during the conditioning session drank mostly saccharin water afterwards,
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close to 100% regardless of whether they were in the control group or the radiation groups. This strong preference for sweet saccharin was also similar in the rats that got saccharin water during training,
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but were not irradiated. Since they didn’t get sick, they didn’t have a US to associate with the sweet taste. The interesting part of this experiment is that rats who received saccharin WITH radiation
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avoided drinking saccharin water later. The more irradiation, the more they avoided the sweet-tasting water. Garcia tested saccharin preference later in these same rats and found that there was strong aversion that lasted 30 days
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and didn’t go back to pre-irradiation levels until 60 days later.
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This seems like a tidy experiment, but you might say, HEY, wait a minute! Did the rats given water while irradiated, these ones here,
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avoid water? Does their saccharin preference indicate that they like sweet taste, or is it that they now hate regular water? Garcia thought otherwise, so he did some more experiments about the nature of the relationship between different types of CSs and nausea-inducing and other aversive events. In classical conditioning experiments, animals have a whole host of sights, sounds, smells, and tastes in the environment to choose from, so which ones get chosen for conditioned taste aversion?

Slide 8: Garcia’s Next Experiment
In another experiment, Garcia and colleagues exposed the rats to a few different types of conditioned stimuli when they drank: in a pre-test they either got water with the sweet taste of the saccharin or a bottle, when licked, that turned on a bright light and noise. They then presented these with different types of aversive events during conditioning.
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Rats were randomly assigned to have all of these stimuli paired with either nausea-inducing x-rays
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or painful electric shocks.
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After conditioning, there was a post-test
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where the rats were given a choice of sweet water OR the tasteless, but bright and noisy stimulus with plain water. This way, they separated the conditioned stimuli to see if they were preferentially associated with particular types of aversive unconditioned stimuli.

Slide 9: Fluid Consumption
The x-ray experiment is shown on the left in blue, and the shock experiment is shown in red on the right. In both cases before conditioning, rats drank roughly equal amounts of the sweet, saccharin water as bright noisy water, showing no strong preference for either. However, AFTER conditioning with the different aversive USs, there was a clear distinction in preference depending upon whether the rat had been conditioned to pain or illness.
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The rats in the nausea condition clearly avoided the sweet saccharin water
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while those in the pain condition
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avoided the tasteless, but bright and noisy water. This shook up the learning world, which firmly supported the idea that conditioned learning is universal, so it shouldn’t matter which stimuli is paired with what. Garcia showed that our sense of taste is more easily conditioned to illness, while our sight and hearing are more easily conditioned to fear.
Garcia’s findings sparked all sorts of debate on Skinner’s and Pavlov’s perspectives on learning. They maintained that the processes of associative learning were universal and general, and that any arbitrary stimulus could be used as a CS, but these conditioned taste aversion experiments showed otherwise.

Slide 10: Conditioned Taste Aversion in Real Life
Garcia’s findings fit with an evolutionary perspective on taste aversion in that it’s important to learn which tastes might make us sick. It’s valuable to learn quickly to associate the tastes and smells of particular foods with nausea, in order to avoid contact with that potentially harmful substance again.
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This knowledge has been used to deter predators, such as coyotes from eating livestock, by placing carcasses laced with lithium chloride,
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a non-lethal chemical that produces nausea, near the livestock they want to protect. Many farms have dramatically reduced coyote predation on sheep herds and turkey farms without trapping or shooting the predators, since the predator’s own natural food aversion keeps them away.

Slide 11: Conditioned Taste Aversion
Hopefully that gives you a clear idea of conditioned taste aversion.

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Tricky Topic: Operant Conditioning

Slide 1: Operant Conditioning
Operant conditioning is basically what most people would call trial and error learning. This type of learning follows certain rules, and this knowledge has allowed us to manipulate conditions to reinforce desired consequences. In fact, it’s a powerful tool that has allowed to collaborate with other animals.

Slide 2: Operant Conditioning: Defined
Operant conditioning is one type of associative learning, where an individual makes a connection between two different stimuli or events. More specifically, it’s learning about the consequences of actions, so is based on voluntary, deliberate behaviours,
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or learning by choosing. What are some examples?
Imagine you just got a new phone, after years of struggling with your old one.
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You decide to text everyone to let them know the good news! You have a general idea of how it works, so you take the instruction booklet
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that came with it and chuck it in the recycling bin.
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You’re going to figure it out all on your own
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by making voluntary responses, like tapping on buttons
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and observing the consequences. If a response results in an unwanted outcome,
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then it’s less likely you’ll do that in the future.
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If another response,
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leads to a favourable outcome,
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then it’s more likely to be repeated in the future.

Slide 3: Early Research: Thorndike
Some of the earliest research in this field was done by E.L Thorndike in the early 1900’s. Thorndike proposed his Law of Effect which states that the consequences of a behaviour increase or decrease the likelihood of it being repeated. This theory was based upon his research with cats in a puzzle box.
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A cat was placed in a box with a lever-operated door, and tasty salmon was placed on the other side. By trial and error, the cats all managed to escape the box by trying different behaviours, and the ones that resulted in desirable outcomes, like pressing a lever that opens a door, were repeated. After a few trials in the puzzle box, the cats escaped very quickly
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once they figured out the best response. B.F. Skinner later coined the term operant to mean any action that operates on the environment to produce specific consequences.
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He invented the operant conditioning chamber, which is usually called a Skinner box. This is an improvement over Thorndike’s puzzle box because it’s designed to measure and manipulate many behaviours; animals tested in a Skinner box can make many responses to obtain their desired consequence, such as pressing a lever multiple times, compared to only one response (escape) in Thorndike’s puzzle box. This is an important innovation because it enables researchers to measure complex concepts, such as the effort an individual is willing to put into a task, by measuring the # of responses an animal is willing to make for a particular consequence. For instance, we know that a hungry rat will make more operant responses for food than a recently fed one, which tells us something about differences in their motivation for food. The Skinner box has been used extensively in many areas of psychology and neuroscience, because motivated behaviour is important for so much: feeding, mating, memory, intelligence, you name it.

Slide 4: Operant Behaviours and Consequences
So here are some examples of operant behaviours, their consequences, and the outcome on future behaviour. Let’s examine 2 behaviours that you might be familiar with. If you post a picture of your cat in Instagram,
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you might be rewarded with loads of likes.
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This behaviour resulted in a WIN for you so the outcome is that you’ll probably post more cat photos in the future.
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How about your morning coffee?
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If your coffee gives you a jolt in the morning so you feel more awake and alert
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and this helps you start your day,
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you’re likely to continue your morning coffee drinking.
Are there rules that govern how we respond to consequences? Sure, lots of them. Through years of research by Skinner and others, we are still learning how this type of learning works.

Slide 5: Reinforcement and Punishment
The most basic rule is whether a consequence strengthens or weakens behaviour.
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Reinforcement is when a consequence INCREASES the occurrence of a future behaviour,
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whereas punishment is when a consequence DECREASES the occurrence of a behaviour.
Reinforcement and punishment both come in two flavours, positive and negative depending upon whether a stimulus is presented or removed. Positive reinforcement
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is when the behaviour results in the addition of a desirable outcome, such as feeling great after exercise.
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People who feel good after exercising will likely repeat that behaviour in the future. Negative reinforcement
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occurs when we respond to get rid of something undesirable,
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such as buckling a seat belt to get rid of the annoying buzzing alarm from the car.
Positive punishment is when a behaviour results in the addition of something undesirable. An example is parking in no parking zone and getting a ticket. This makes that behaviour less likely to be repeated in the future, lesson learned. Negative punishment is when a behaviour results in the loss of something desirable
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such as when a kid uses bad language where their parents can hear, and they lose all screen time for the day. The intent of this is to reduce the swearing behaviour.

Slide 6: Types of Reinforcers
Reinforcers are rewards or incentives that guide behaviour in the direction so we get what we want. But what do we want? There are some reinforcers that are universal, in that everyone finds them innately rewarding or aversive.
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Primary reinforcers are those that do not require prior learning, since they satisfy some instinctual need. Examples of a positive, primary reinforcer is food
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especially when we’re hungry and the food is tasty. Pain
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is a universal primary, negative reinforcer in that all animals will engage in behaviours that reduce or avoid it. Secondary reinforcers,
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also called conditioned reinforcers, are not inherently rewarding or aversive, they are meaningful because they are associated, in past experience, with a primary reinforcer. A fantastic example of a positive, secondary reinforcer is money
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like these bills here. If I told you that you could pick one, you would likely take the hundred since its worth more money, rather than the much prettier $50 or $10. An example of a negative, secondary reinforcer is a low grade on a test,
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which should hopefully strengthening studying behaviour to avoid getting this grade on the next test.

Slide 7: Operant Conditioning in Real Life
Understanding operant conditioning is actually very useful in real life, as anyone who has tried to train a dog will tell you. Our knowledge of how operant learning works has allowed us to tap into the superpowers of other animals, like dogs’ amazing sense of smell. By rewarding detection of certain substances, like explosives, with a treat, dogs are able to operantly learn about behaviours and consequences in a way to make us safe. A combination of threats and bribes are quite often used to shape the behaviour of lots of animals, including humans
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as every parent knows. Addictive drug-seeking and drug-taking behaviours also follow the rules of reinforcement and conditioning,
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so many successful treatments incorporate classical and operant conditioning principles to “untrain” problematic behaviours.

Slide 8: Operant Conditioning
Operant conditioning allows us to make decisions about based on how past behaviours worked out. Knowing the principles of reinforcement and punishment are powerful tools in training ourselves and other animals.

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Tricky Topic: Schedules of Reinforcement

To be updated at a later date

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1032 Tricky Topics

Tricky Topic: Nature of Language

Slide 1: Nature of Language
Language is critical part of how humans work with information, so we’ll consider the nature of language.

Slide 2: Human Language
Human language is a system of communication specific to Homo sapiens. Most animals communicate, but they’re only able to convey immediate concerns and concrete states, like being angry, threatened, hungry, hurt, or eager to reproduce. So what makes our system of communication different than other animals?

Slide 3: Human Language Forms
Unlike BOOM or MEOW, most word sounds don’t bear any relationship whatsoever to the things they’re describing. So, the words in human language are symbolic. These symbols differ between languages, so there’s a lot of variation in the sounds different groups of humans use to communicate – there are about 5000 languages spoken in the world today. We think of language as spoken or written, but some languages, like American Sign Language, are completely based on gestures.
With so many forms of this symbolic system, human language is very flexible. This openness to communicate different meaning is probably the biggest difference between language and other forms of animal communication. ALL known humans use language to communicate, and there are some universal rules amid all this variation.

Slide 4: Components of Language
Lexicon refers to all the words in a language, this includes everything in the dictionary AND everything that’s not.
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Grammar refers to the set of rules for conveying meaning, using words from the language’s lexicon. These two components provide the structure for language, so others who know the same system can understand. For instance, most plural words in English end with the letter “s” while in Turkish plural words end with either “ler” or “lar.” Even though grammatical details differ between languages, the use of these rules is universal. From these two foundational components, language is an incredibly flexible communication system and allows humans to talk about events not tied to the present moment.
Let’s consider some other components of language, by using an example. Take this sentence
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“I talk too much.” Although you can see that there are four words here, there are more than four sounds. First is the “I” sound of the first word,
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then the “t” sound of T,
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the “aw” sound of A,
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and the “k” sound of K.
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Note I didn’t include the silent L, since it doesn’t contribute to the sound of the word talk. In the word too there’s another “t” sound with T
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and an “oooo” sound from the two Os
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Much starts with the “m” sound of M
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then “uh” from U,
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followed by the “ch” sound from CH.
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This sentence has four units of meaning,
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”I” is the subject of this sentence,
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talk is the action happening,
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too conveys excess, and
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much indicates amount.
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These are called morphemes, or units of meaning in a language.
In this sentence each word is also a morpheme, but that’s not always the case. This similar this similar sentence
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”I talked too much” Has four words, but five morphemes. Can you find the extra one?

Slide 5: Language and Thought
The benefits of language as a communication system are obvious, it allows humans to talk about the past and future, and even things that have never happened. It allows us to easily share memories, and therefore knowledge.
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With 5000 different languages, there are a lot of ways to say things. Does that mean that there are different ways of thinking about things?
There is some evidence for this, by looking at how languages with different attributes influence people’s judgements.

Slide 6: Linguistic Relativity
Linguistic relativity, originally called linguistic determinism, is the idea that language influences the way we think.
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This perspective is also called the Sapir-Whorf hypothesis after Edward Sapir and his student, Benjamin Lee Whorf. Evidence to support this was mainly from comparisons of speakers of different languages. Some languages have more words in their lexicon to describe concepts like colours,
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so one approach is to compare participants’ performance on a colour categorization task.
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Whereas English has only one word for the colour category blue, Russian has two words depending upon whether the blue is light or dark.
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One study asked native English and Russian speakers to categorize colours;
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they were shown a square like the one on the top, and then had to choose one from a pair (shown on the bottom). For the Russian speakers, when the blues were in different colour word categories, they made faster discriminations, but the English speakers did not. This shows using an objective categorization task, that having words for a category made the task easier.
So there is some evidence of an influence of language experience on perceptual tasks, but these differences tend to be small and restricted to certain types of tasks. That’s why the term linguistic determinism fell out of favour, and linguistic relativity is more commonly used.

Slide 7: Nature of Language
The structure of language and collection of words allow information to be shared with others. This allows for variability and flexibility that makes human language much more powerful than other animal communication systems.

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Tricky Topic: Heuristics

Slide 1: Heuristics
In this lecture, we’ll explore the importance of heuristics in decision-making.

Slide 2: Making Decisions
The average human makes countless decisions every day, and most of these happen without our notice. Each decision we make involves processing information as efficiently as possible, so that we can free up our minds to do the next thing. Decision making is all about problem solving, which sometimes we do very well, and other times really poorly because we rely on certain strategies that lead to mistakes. There are many different problem-solving strategies available to us, so let’s look at some common ones.

Slide 3: Problem Solving Strategies
An algorithm is a step-by-step procedure for solving a problem. They’re powerful because they’re thorough, so are designed to generate the BEST answer. Computers, with their massive processing speeds, use software algorithms a lot. A downside for humans is that they’re time-consuming, so we don’t use them as much.
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We sometimes arrive at sudden solutions in a flash, referred to as a Eureka insight, which is the word Greek mathematician Archimedes shouted when he realized the principle of volume displacement while taking a bath. These flashes of insight are unpredictable, so aren’t reliable tools in our day-to-day problem solving.
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We’re much more likely to use mental shortcuts called heuristics. Let’s look at an example.

Slide 4: Unscramble This
What word can you make from these eight letters? Take a minute and see if you can unscramble it, pause the video if you like. Did you get it? In fact, there are over 40 000 ways to rearrange these letters, so using an algorithm to check every single one against an English dictionary would take forever for a slow human brain. One way to try and solve this problem is to apply some shortcuts,
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..like placing the “s” at the end, since this is how we form plurals in English. Also, most words start with consonants rather than vowels so you can quickly eliminate quite a few of those 40 000 possibilities by ignoring the combinations that start with vowels. Eventually you’re likely to come up with the answer

Slide 5: Answer
RAINBOWS.
It’s easy to see from this simple example how we use heuristics for these types of problems, but it wasn’t until recently that our reliance on these mental shortcuts became widely accepted.

Slide 6: Rational Choice Theory
For most of the 20th century, Rational Choice Theory was the prevailing view of psychologists, economists, and others who studied decision making. This is the idea that humans make RATIONAL choices to best reach their goals. At the time, most experts believed that decision-making was based on cost-benefit analysis;
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weighing the costs associated with a course of action with the predicted rewards. However, in the early 1970s,
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2 Israeli psychologists, Daniel Kahneman and Amos Tversky, challenged rational choice theory. They felt that people make all sorts of NON-RATIONAL decisions and demonstrated this with some simple studies.

Slide 7: Challenging Rational Choice Theory
In one experiment participants heard 39 names, 19 famous women and 20 non-famous men. Then they were asked which gender they heard more frequently.
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Most people, 80%, claimed that they heard more female names, presumably because the famous names were more memorable. This tendency to solve problems based upon how easily we can pull information into our awareness is called the AVAILABILITY heuristic. And it’s something that we use ALL the time.
Tversky died in 1996, but Kahneman was awarded the Nobel Prize in Economics in 2002,
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based on their work on biases in judgement and decision-making.

Slide 8: What Would You Do?
Let’s say that you’re late for class and you can see up ahead that the crosswalk light is telling you to stay put. What do you do?
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Your brain might quickly recall times when you’ve jaywalked in the past and nothing happened, and so decide to charge on ahead.
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OR, you might remember that there were a number of crosswalk accidents recently and decide to play it safe and stay put. Either way, we make these quick decisions all the time, based on the information that is AVAILABLE to us. So, under what conditions are we likely to use the AVAILABILITY HEURISTIC?

Slide 9: Availability Heuristic
One factor is vividness. In other words, if I can imagine it, it must exist. In one study people were asked to estimate the likelihood of dying from various causes, and most people said that death from a tornado was much more likely than dying from asthma.
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In fact, this is totally wrong, asthma kills many more people, but tornadoes are dramatic events, and are much more easily called to mind.
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Another source of availability is our recent experiences. Events that receive a lot of media attention can bias our thinking and lead us to make incorrect judgments. In other words, if everyone is talking about it, it must be everywhere. For instance, leading up to the 2016 summer Olympics in Rio,
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there was a lot of news coverage about the mosquito-bourne Zika virus, linked to birth defects in newborns. Sales of mosquito repellants rose dramatically, even in areas where the risk was very low.
According to Kahneman and Tversky, we have a tendency to rely on this way of thinking when we’re uncertain. But what about situations where have solid information to help us solve a problem?

Slide 10: What are the Odds?
Let’s say we have a container with 20 red chips and 80 white chips. If you put your hand in and pulled out a chip at random, how likely is it that you’ll get a white one?
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Most people correctly answer 80%.
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What about the chance of getting a red chip?
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Again, most people would correctly answer 20. But let’s make this a little more interesting.
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Let’s say we have a container with 20 lawyers and 80 engineers. Again, if you put your hand in and pulled out a person at random, how likely is it that you’ll get a an engineer?
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Most people correctly answer 80%.
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What about the chance of getting a lawyer?
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Again, most people would correctly answer 20. BUT the interesting thing is that people throw this logic out the window if they’re first given a personality description.
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So, if instead I told you that we randomly pulled someone out of this collection of 100 people, and that this person likes to argue, is very good at debating, and is considering a career in politics, would this change your estimate? Do you feel like the odds now are MORE than 20%. Most people when given this description, say it’s more likely that this person is a lawyer, since it fits the common stereotype of a lawyer. However, the odds HAVE not changed, the likelihood remains 20%. This type of mental shortcut is known as the representativeness heuristic.

Slide 11: Representativeness Heuristic
When using this heuristic we estimate the probability of an event based on how typical it is of another event. We think of certain occupations having representative behaviours, so it can lead us to ignore other information. Because debating and politics are common interests for many lawyers, this can lead us to use the representativeness heuristic and bias our assessment of the random draw.

Slide 12: Heuristics
These are just TWO examples of heuristics. They save us time so often come in handy, but they are inherently biased so can also lead us to make mistakes.

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Tricky Topic: Measuring Intelligence

Slide 1: Measuring Intelligence
This Tricky Topic discusses how intelligence is measured and how we have arrived at the current paradigm of intelligence testing. Before getting into how we measure intelligence, we must first ask what is intelligence?

Slide 2: What is Intelligence?
What are we really measuring when we talk about intelligence? What do we currently value in society as being intelligent?
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Is it the mathematical mind of Einstein?
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Or perhaps the artistic genius of Picasso? Or is it both? Nevertheless, it is important to understand how society’s views on intelligence have changed and how, as a result, the testing of intelligence has changed as well.

Slide 3: Theories and Measurements (1910-1980)
If we look back at the history of IQ testing, we see that it has changed and evolved for both practical and theory-driven reasons. Where in general, the history of intelligence tests can be divided into 3 distinct historical periods. Intelligence testing as an idea was first coined in 1865 by Sir Francis Dalton in England. However, it wasn’t until the early 1900s that intelligence was first measured in a practical and clinical context.
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The 1st practical test was devised by French psychologist Alfred Bennet.
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And this was a test that he made consisting of 30 problems of increasing difficulty,
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where the score was then determined by the patient’s mental age divided by the chronological age multiplied by 100, which gave a score referred to as the intelligence quotient or IQ.
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And this method of scoring very clearly become problematic across different ages
For example, let’s say you have a 30 and 40-year-old man. To begin,
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let’s say the 30-year-old man scored a 30 on this test. So let’s say he has a mental age of 30 and a chronological age of 30,
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so his score would therefore be his mental age divided by his chronological age times 100, which gives a score of 100 for his IQ.
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This contrasts with the 40-year-old man who has a score of 30 on the test as well, so that is a mental age of 30 and a chronological age of 40, where his score would come out to an intelligence quotient of 75. So even though these 2 men did exactly the same on the test itself, because of their difference in age, the 40-year-old man had an IQ score three quarters that of the 30-year-old man’s score.
So this problem is evidently very prominent and became addressed in the 1930s by David Weschler.
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And David Weschler distinguished between adults and children as having fundamentally different cognitive abilities and he devised respective intelligence tests for children and adults, allowing for the negation of chronological age in scoring. David Weschler devised 2 tests. The first one is the Weschler adults intelligence scales,
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with the second being the Weschler intelligence scale for children.
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Slide 4: Theories and Measurements (1980’s)
Now, the second era of intelligence testing came in the 1980’s with the Kauffman assessment battery for children. And this was an intelligence test that directly challenged the Weschler intelligence test in 4 specific ways.
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The first being that it was guided by theories of fluid and crystallized intelligence and Piaget’s theory of cognitive development.
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The second, it recognized fundamentally different intelligence characteristics for different ages amongst children.
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The third, it measures several distinct aspects of intelligence.
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And finally, it assessed different types of learning styles.

Slide 5: Theories and Measurement (1990’s)
So following this, the third and current era came in the 1990’s, for intelligence tests began to recognize the many different facets and measures of intelligence. So Carroll took Cattell-Horn theory and analyzed all known intelligence tests linking different models on intelligence from single qualities to multidimensional models. This has set up the current paradigm of intelligence tests that assess different forms of intelligence.
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So, for example, we’ll look at the fourth version of the Weschler adult intelligence scale and the Weschler intelligence scale for children that was released in 2008. And these tests now include 4 different dimensions of intelligence.
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Verbal comprehension,
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perceptual reasoning,
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working memory,
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and processing speed. So, now that we understand what the current paradigm of intelligence tests are actually measuring, it is now important to look at and address how individuals are scored and ranked within current intelligence tests.

Slide 6: Current IQ Testing
We cannot describe the scoring of IQ tests without first discussing the very basic ideas behind the theory referred to as the central limit theorem. This is a part of the probability theory. And to define it, the central limit theorem states that a group of independent, random variables of a significant quantity will be normally distributed. And this sounds like a mouthful, but we’ll try and highlight this in the next example, where we’ll look at the heights of individuals in a certain population. So, when we look at a group of individuals,
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each person’s height is independent of all others as well as random within the population.
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So if we then took this group and began to bin them based on their heights, according to the central limit theorem, they would follow a specific type of distribution as these individuals are both independent to one another and random within the group. And again, the distribution they would follow is termed a normal distribution.
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So, if we then plot the heights of all the individuals in the population into a histogram, as you can see here, and then plot the curve of this histogram, we should see what is described as a bell curve. It is important to know that the bell curve on the histogram becomes smoother and continuous as the number of individuals in the population we’re looking at increases.
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Where a really large population following a normal distribution would look more like this curve: extremely continuous and smooth. And to look further into a normal distribution, what we see is that there are 3 main characteristics that hold true across all population measures that are shown to be normally distributed.
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The first being that the mean, median, and mode are all equal.
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The second being that the distribution is symmetrical- 50% of the data or individual counts fall on either side of the centre.
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And finally, the distribution is uniform such that the SD, which is the measure of how spread out the numbers are from the mean, is constant in a normal distribution such that one SD encompasses approximately 68% of individuals,
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2 SD encompass approximately 95% of the individuals,
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and 3 SD encompasses approximately 99.7% of the individuals within that normal distribution.
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So now, just like the heights of individuals, we can also use IQ scores on a frequency plot that will be normally distributed. That is, IQ scores of individuals also follow a normal distribution where in this case they have a mean of 100
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and a SD of 15.
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So scores from 85-115 are termed average.
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Scores less than 70 are extremely low.
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Scores greater than 130 are very superior.
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As a quick example, let’s say you score 115 on your IQ test.
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So this means that you have an above average score that is within the 84th percentile, meaning that you fall in the top 16% of scores.

Slide 7: Measuring intelligence
This tricky topic covered both what intelligence tests are measuring and how individuals are scored and ranked relative to others based on their IQ. Thanks for listening.

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Tricky Topic: Validity and Reliability

Slide 1: Validity and Reliability
This Tricky Topic covers the concepts of validity and reliability, and specifically relates these two terms to the IQ test.

Slide 2: How useful is a test?
In almost all aspects of our lives, our merits and values are judged or determined by some sort of test or assessment. From a very young age, we are tested all the way from the classroom to the doctor’s office where you might need a new pair of reading glasses. And in of all these tests we perform and are subjected to throughout our lives, it is important to ask, “how useful is this test?”, or “how useful are the results this test is producing?”.
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So, for example, how good of test is bench press for athletic ability such as football? Should the NFL and CFL teams be using this as a measure for which players they draft or not?
Or can measurements of the human skull really tell us about the individuals’ brain and therefore mind within? We’ll come back to this example in more detail at the end of this tricky topic

Slide 3: Validity
We can begin to answer these very important questions with 2 different concepts, those being validity and reliability. To begin, validity
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is asking the question “how well does the test actually measure the concept (or construct) that it claims to measure?”.
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So, for example, is holding a measuring tape to the sky a valid way to measure the circumference of the sun? As we all should know, this is not a valid way to measure the sun. The results from this method of measurement would be completely unrepresentative of the true circumference of the sun and we know that there are much more valid ways to do this measurement, like using the proper mathematical formula
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So, bringing this into the context of IQ tests, when measuring the validity of an IQ test
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we would ask “does a person’s IQ score accurately represent their intelligence?”.
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This question is obviously very important and can be broken down further into 2 specific subsets, that being construct validity
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and predictive validity.
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So, to begin, construct validity
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is asking the question: “does a test measure the concept or construct it’s claiming to measure?”. So, for example, does an IQ test actually measure intelligence? Similar to what we just stated in the previous slide. The second being predictive validity,
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asking, “how well do test results or IQ test results positively correlate to real world outcomes?”. Coming back again to the example of IQ tests,
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do IQ scores correlate with school grade achievements and job success?
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In terms of predictive validity of the IQ test it actually has a very high correlation with school grades all the way from junior kindergarten to university.
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However, it does not predict happiness or satisfaction along the lifespan.

Slide 4: Reliability
The next measure that we use is reliability.
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Reliability addresses the consistency of the results. It asks, “how often will a test yield the same results under the same conditions”.
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To begin, for example, the roll of a standard die will not have good reliability for getting the same number twice in a row. It will have a 1 in 6 chance to roll the same number twice with the die.
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Another and perhaps more exciting example could be getting a hole in one in golf.
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Most golfers have met another golfer or perhaps themselves who has hit a hole in one before. But it’s important to ask yourself “what do you think the likelihood that one of these people or yourself could hit another hole in one?” or “do you think the fact that a golfer has hit a hole in 1 before is a good measure of their day to day golfing ability? Is this one incident reliable enough that you can conclude anyone who has hit a hole in 1 before could play at the level of Tiger Woods, let’s say?”
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The answer to this question undoubtedly is no, and the reliability of hitting a hole in 1 is therefore not very high and does not equate to being a world-class golfer like Tiger Woods.
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So, in contrast to these last 2 examples, the reliability of the IQ test is actually extremely high. On a scale of 0-1 the IQ test has a correlation coefficient of 0.9.
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The test-retest reliability of the IQ test is very high, meaning that if you take the test again there’s a very high chance that you will get the same score again. This has been shown to be true even over a number of years. Another important concept is internal consistency,
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which is also very high on IQ tests. This measures how well the questions on the test are assessing the same dimension aligned with one another. For example, does a person get the same relative result on question 1 and question 2 if both questions are aiming to measure working memory? Well on the IQ test, the answer is yes.

Slide 5: Validity & Reliability
So, in review, coming back to our initial question, “how useful is a test?”, we have 2 main ways to assess this question. That is, validity and reliability. We’ll go back to the one example we briefly talked about earlier, where we asked about the usefulness of measuring the dimensions of a skull to learn about the inner workings of that person’s mind.
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And this is a practice called phrenology that was used fairly commonly in the beginning of the 19th century and this is a perfect example of how tests can be reliable while being completely invalid. The test retest reliability of phrenology is very high, as the bumps on a person’s skull will not change much or at all from one examination to another. HOWEVER, the validity of the practice is completely absent, as in no way do the bumps on a person’s skull measure or give insights into the inner workings of their mind.
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That concludes this Tricky Topic looking at validity and reliability. Thanks for listening.

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Tricky Topic: Developmental Research Designs

Slide 1: Developmental Research Designs
Childhood is a time of change, so developmental researchers use special types of designs in order to capture and compare these changes. We’ll consider three types of designs, cross-sectional, longitudinal, and longitudinal-sequential

Slide 2: Age-related Changes
Identifying age-related changes is key in the study of development. Measuring variables as they change over time means chasing a moving target. Developmental psychologists use different strategies to address this challenge, each with their own advantages and disadvantages.

Slide 3: Cross-Sectional Design
A cross-sectional design examines different aged participants at the same time.
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Once groups of participants are identified and recruited the behavior of interest is measured, for example, the amount of time spent on the internet.
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Cross-sectional designs are the simplest of the developmental research design types, because all participants can be tested at once, however this comes with an important limitation. Each age group, called a cohort, in a cross-sectional study grew up at different times in history, and this means different political, societal, parenting norms.

Slide 4: Cross-Sectional
One of the biggest differences over the past few decades is advances in technology so children born years apart likely have different exposure and access to it A hundred years ago, radio was the most sophisticated form of social media, whereas today most people have immediate access to all knowledge ever known at our fingertips.
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This is called a cohort effect and could certainly influence the results of our proposed study of age-related differences in time spent online.
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If we find differences, it’s impossible to determine if they’re related to age alone, or if this is a product of the technological opportunities while growing up.

Slide 5: Longitudinal Design
One way to overcome cohort effects is by using a longitudinal design, where the same group of individuals is tested over time. Let’s consider our earlier study of age-related differences in internet use.
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We can start with a group of six-year olds, then wait two years and test them again at age 8, and then again at age 10.
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This gets around the cohort effect, since all children are drawn from the same cohort. One obvious disadvantage is that this takes a much longer times than a cross-sectional design. This usually makes the study more expensive since participants need to be contacted again and again. Also, there is problem with attrition, or loss of participants from the original sample over time, which is inevitable people move away or are no longer interesting in participating at later time points.

Slide 6: Longitudinal Sequential Design
The most comprehensive design is a longitudinal-sequential (or sometimes called just sequential) design. This combines both the cross-sectional and longitudinal approaches, to overcome the limitations of both. Let’s look at how we can fit our original question of internet use into this framework
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Let’s look at children from two cohorts, those born in 2012 and 2014. If we test them together in 2020
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we’d have a group of 6 year olds and 8 year olds
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At that point we could do a cross-sectional comparison. If we wait two years and test the same children again, we now have a group of 8 year olds and 10 year olds
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We can do another cross-sectional comparison,
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but we also have the ability to do a longitudinal comparison in the same participants.
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Note that we can also compare age cohorts born in different years
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If we test again two years later, we have a group of 10- year olds and 12-year olds
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and we can make those three comparisons again
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So this type of design is incredibly powerful since it can disentangle age-related changes from cohort differences.
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However, this research design is not used often, because it’s very time-consuming, expensive, and of course with several groups followed over time there is a great chance of attrition.

Slide 7: Developmental Research Designs
The continual change that happens early in life means that special research designs are required.

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Tricky Topic: Piaget’s Stages of Cognitive Development

Slide 1: Piaget’s Stages of Cognitive Development
This Tricky Topic discusses Piaget’s stages of cognitive development, outlining his theories of early cognitive development in particular.

Slide 2: Early Cognitive Development
Early cognitive development was extensively studied by Jean Piaget.
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He studied early infant and childhood advances in the ability to think, pay attention, reason, remember, learn, and solve problems.
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In particular, he mostly studied attention.
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And this is because attention can be observed and measured in all ages, even when the individuals are too young to communicate via language or other means.
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The main question Piaget asked himself was “how does a child’s thinking develop?”. His interests and life’s work trying to answer this question stemmed from the simple observation that children often answer simple questions wrong at different developmental stages and Piaget wanted to know in what way do children think that makes them answer these questions wrong. As mentioned, Piaget thought a potential doorway into answering this question was by studying a child’s attention. He viewed all children as actively constructing knowledge about their world by forming schemas with new experiences.
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Now, schemas are very important. They are mental representations of aspects of the world which provide a framework for understanding the world. There are 2 important mechanisms for schema formation.
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They are assimilation and accommodation.

Slide 3: Schemas
Assimilation is fitting a new experience into an already existing schema when children encounter something new. Accommodation is the process by which a child will change an existing schema to incorporate new information. For example, say a child sees a donkey for the first time.
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With assimilation, the child might fit the donkey into an already existing schema they have of a horse, for example.
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Whereas if the child used accommodation, the child would change the existing schema of the horse, acknowledging that this is actually not a horse, but indeed a donkey.

Slide 4: Jean Piaget
Once again, it’s really important to illustrate that Piaget’s primary focus was infant thought. He did this by looking at their ability to form new schemas for novel and unfamiliar stimuli by looking at their focus and attention.

Slide 5: Piaget’s Stages of Cognitive Development
It was based on these specific observations of children that Piaget formed his idea of early cognitive development in which he came up with 4 distinct phases of cognitive development from birth through adolescence.
These were first the sensorimotor stage,
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which lasts from about birth to 2 years old.
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Next was the preoperational stage from about 2-5 years old.
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And then the concrete operational stage from 6-11,
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and then finally the formal operational stage from ages 12 and up

Slide 6: 1) Sensorimotor Stage (0-2)
To begin, in the sensorimotor stage, Piaget claimed that the knowledge that a child or an infant gains is through the senses, that is through tasting, smelling, seeing, touching, and hearing.
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One phenomenon that Piaget believed to be indicative of these early stages and in particular the early stages of the sensorimotor stage was the lack of object permanence. And that is an absence of the ability to recognize that objects still exist when they are not being sensed. One way to judge is this is to have an object of interest in front of an infant and then put a cloth or some other object in front of it. For the first 8-9 months infants will not understand the object of interest is still present, but just on the other side of the blocking object

Slide 7: Preoperational (2-5)
In the second and preoperational stage of cognitive development Piaget believed that certain qualities of thinking began to develop. The first being symbolic thinking, that is using symbols such as words or letters to represent ideas or objects.
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The second is animist thinking. This is the belief that inanimate objects are alive. For example, children might think of the sun as alive because it follows them when they walk. In addition, they might think that their stuffed teddy is a real bear.
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The third is egocentrism, which is to view the world from one’s own perspective while unable to view it from another person’s perspective. This theory can be illustrated by one of Piaget’s classic experiments referred to as the 3 mountains task. In this experiment, 3 slightly different mountains are arranged on a table, with the child on one side and a doll on the other. The child is given 3 options of drawn perspectives and asked to pick the one that the doll was likely looking at. A child in this stage will pick the perspective they themselves are seeing every single time, as they are unable to imagine what the doll’s perspective might be.
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Finally, the fourth is a lack of conservation- absence of the ability to recognize that some properties of an object can change while others remain constant. For example, children in this stage lack conservation of liquid.
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If they see 2 equal glasses with the same amount of liquid in each glass, they will recognize that the amounts of water are the same.
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However, if you then in front of them pour the water from one of the glasses into a petri dish,Click
they will now say that the glass has more water because it’s bigger, even though the amount of water never changed from the glass to the petri dish.

Slide 8: Concrete Operational (6-11)
This leads into the 3rd stage, which is the concrete operational stage, where children can now conserve shape, number, and liquid. If looking at the previous problem, children will now identify that even though the size of the container is different, the amount of water between the glass and the petri dish is the same. However, this ability is limited to mental observations of real or concrete objects and events. In this phase they still cannot understand abstract ideas and reasoning. For example, they have a hard time with the worded questions where they have to imagine objects. Let’s look at the following written example.
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Let’s say a child was asked, if you have water in a small cup then you pour it into a bigger cup, which cup has more water?
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They would answer the bigger cup in this stage of development.

Slide 9: Formal Operational (12+)
Lastly in the 4th formal operational stage, formal logic develops. For example, a child in this stage could ration that if Maria is a woman, and all women are mortal, then Maria is mortal. In addition, children develop scientific reasoning and hypothesis testing skills during this stage.

Slide 10: ???Piaget’s Stages???
So before finishing, let’s look at the following experiment. This experiment is one example illustrating an infant’s ability to understand basic statistics and probability.
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Researchers in this experiment took many black balls and very few red balls and put them into a box in front of 8-month old infants. It’s really important that they did it in front of the infants such that they could see the proportion of black to red balls. The idea is that the infants were actually able to see and recognize the different proportions of the black balls and the red balls and therefore make basic statistical predictions based on these.
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The way this is illustrated was the researchers then put their hands into the box and would pull out different combinations of red and black balls. So, when researchers pulled out an expected hand of many black and very few red balls,
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babies would pay little attention. However, when researchers pulled out many red and few black balls,
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babies spent a significant amount of time focusing on that hand. So, researchers therefore concluded that the babies were recognizing this as an unlikely event, suggesting that they understood the basic premise that a sample group from the box should reflect the contents of the full box, which in this case they knew was many black balls and few red balls.

Slide 11: Piaget’s Stages of Cognitive Development
This concludes this Tricky Topic looking at Piaget’s stages of cognitive development. Thanks for listening.

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Tricky Topic: Prenatal Development

Slide 1: Prenatal Development
This Tricky Topic discusses the phases of prenatal development as well as how teratogens can interfere with these phases, producing lifelong effects.
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By the time a baby is born, the amount of growth and development it has already gone through in the womb is incredible! Although babies first enter the visible world when they are born, their journey of growth begins well before they first open their eyes.
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We begin with a single cell
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forming an organism that undergoes extreme growth and maturation
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in the mother’s womb to form the baby we see at birth,
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which is comprised of billions to trillions of cells. It is the stages of development before the baby is actually born that we are going to focus on for this tricky topic. This process is referred to as prenatal development.
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Prenatal development can be broken down into 3 major stages. The first is the germinal stage,
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which lasts from conception to about 2 weeks post-conception. This is followed by the embryonic stage
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which lasts form the 2 weeks to 8 weeks post conception, and then finally the fetal stage
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which lasts from about 8 weeks post conception to birth.

Slide 2: Germinal Stage
To begin, the germinal stage begins when the eggs are released from the ovary entering and moving down the fallopian tube within the potential prospective mother. Subsequently, during intercourse, sperm cells swim up the fallopian tube to meet the eggs. While many sperm cells surround and egg, only one will succeed in penetrating it, a process known as fertilization.
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It is at this point that the sperm and the egg come together to form a zygote.
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The zygote then continues down the fallopian tube while going through many subsequent cell divisions, growing in size and density. At approximately 4 to 5 days, the zygote has formed into a blastocyst that enters the uterus.
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Following this, at about 11-12 days the blastocyst implants into the uterine wall and this is a critical stage where about 30-50% properly plant, and therefore the pregnancy ends. However, when this is successful and the blastocyst implants into the uterine wall,
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it sets up the next stage of embryonic development.

Slide 3: Embryonic Stage
And this being, the embryonic stage. So, once a blastocyst implants into the uterine wall, the embryonic stage begins. At this point the growing bundle is termed an embryo. In particular this stage is marked by the formation of major organs, including the nervous system, the heart, eyes, ears, arms, legs, teeth, palate, and external genitalia. The embryonic stage until about 8 weeks after conception, where it then leads into the fetal stage.
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The fetal stage is marked by the formation of bone cells. In addition, at this point, major organs have already formed. For example, the heartbeat can first be detected around 8 weeks. So, from here until birth, organs continue to grow and mature, producing a rapid growth in the embryo’s size. So now that we’ve briefly gone through the stags of prenatal development, there is a very important concept we need to address.

Slide 4: Environmental Influence on Fetal Development
That is that the environment is extremely important because it has great influence on fetal development. This really illustrates the temporal importance of certain developmental conditions and periods. During prenatal development the fetus is completely dependent on the environment of the mother’s womb. The factors within the mother’s womb come from many sources, including what the mother eats,
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drinks,
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smokes,
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feels, and experiences. And it is the collection of these factors forming the environment of the worm that governs the fetus’s development. This is referred to as prenatal programming.
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Prenatal programming is the process by which the events in the womb alter the development of both physical and psychological health for both the newborn baby
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as well as the subsequent adult.
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With respect to negative effects, damage can be caused either by a lack of factors necessary for proper development or by the introduction of factors that actively interfere with proper development.

Slide 5: Teratogens
And this brings us to teratogens. These are substances and chemicals that come from the external environment and have a negative impact on fetal and infant development. The severity of the effects of teratogens is time dependent.
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For example, certain teratogens have greater effects when consumed at a specific period of prenatal development. The severity of the teratogen of the subsequent effects is dependent on the timing at which this teratogen is introduced. In general, the earlier the exposure to a teratogen during a pregnancy, the greater the effect. Several substances are known teratogens.
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These include nicotine, caffeine, alcohol, and some prescription drugs, just to name a few. These have all been shown to have major negative effects on prenatal development.

Slide 6: Prenatal Development
That ends our Tricky Topic on phases of prenatal development and how the environment can affect these phases. Thank you for listening.

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Tricky Topic: Myelination of the Prefrontal Cortex

Slide 1: Myelination of the Prefrontal Cortex
Although the brain of a six-year-old will look similar in size and appearance as the adult brain. The neural connections within the brain continue to develop throughout adolescence and well into adulthood.

Slide 2: Myelination of the Prefrontal Cortex
The myelination of the neural pathways within the prefrontal cortex is one of the final steps to transform a teenage brain into a fully matured adult brain.

Slide 3: Myelination of the Prefrontal Cortex
Myelination refers to the formation of a myelin sheet around the axons of neurons. The glial cells of the central nervous system called oligodendrocytes produce the myelin sheets, which are a fatty substance that wrap around and insulate neuronal axons. Myelination is a crucial adaptive process since it strengthens and accelerates the electrical transmission between neurons, thus coordinating how well brain regions work together.

Slide 4: Myelination of the Prefrontal Cortex
After birth, the population of oligodendrocytes drastically expands and there is a wide spread of myelination happening throughout the first two years and this gradually continues into early adulthood.

Slide 5: Myelination of the Prefrontal Cortex
However, the rate of myelination within the brain follows a distinct spatial temporal pattern. Specifically, myelination will start at the brain stem regions and move upwards from the back of the cerebral cortex towards its front. This pattern closely mimics the evolution of the brain in which the more primitive structures will undergo myelination first and the structures associated with conscious thought and higher cognitive function will be myelinated last. As a result, the prefrontal cortex is the last brain region that gets fully myelinated. Although most brain regions will have already received a surge in myelination prior to reaching adolescence, the prefrontal cortex will only begin its rapid increase in myelination after puberty and will only reach its full maturation until early adulthood. This has many implications when it comes to understanding the risk-taking behaviour and poor emotion regulation that teenagers will often demonstrate.

Slide 6: Myelination of the Prefrontal Cortex
The prefrontal cortex is heavily connected to other brain areas and is responsible for a variety of higher-level cognitive functions or what is commonly referred to as executive functions such as planning and decision making, controlling emotional impulses, attentional control, and the ability to conceptualize long term goals. Therefore, during adolescence, the neural networks responsible for these functions are still being refined and constructed by the process of myelination. Consequently, these networks are far from perfect.

Slide 7: Myelination of the Prefrontal Cortex
Think back to your early teenage years. I bet you can think of many examples in which you would now seriously question the decisions you made, whether it be engaging in risky behaviour that you would never consider doing now or having absolutely no control over your emotions or simply being easily distracted are all behaviours that can be associated with the lack of prefrontal myelination. It is for this reason that once we reach our early twenties or for some, it might take a bit longer, that we can plan things more effectively, handle our emotions in a healthier manner, and overall become better thinkers.

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Tricky Topic: Theories of Motivation

Slide 1: Theories of Motivation
Why do we do the things we do? Why are we drawn to certain activities and behaviours? In this Tricky Topic, we’re going to dive into the muddy waters of motivation.

Slide 2: Motivation
Studying motivation is essentially exploring what individuals WANT. When faced with making a decision, our WANTS have a huge voice in what we actually decide to do. We make hundreds of little decisions every day, possibly thousands. Some of these are deliberate and take years , like choosing what kind of career to pursue, while others are more spontaneous and unplanned, like the kinds and amounts of food we choose to eat.

Slide 3: Motivation Defined
Motivation is defined as wants or needs that direct behavior toward a goal. There are a couple of terms that are used to describe different aspects of motivation which will be useful in comparing theories.
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A need is commonly defined as a biological state of deficiency that triggers drives.
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A drive itself is a subjectively perceived state of tension that occurs when deficient in something. Therefore, drives are need-specific.
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An incentive is any object or event that motivates behavior. This is another word for a reinforcer, or something that increases the likelihood of a behaviour happening. An incentive can trigger motivated behavior without a true biological need.
Whereas drives PUSH behaviour, incentives pull behaviour, and so there are both internal and external forces that can feed into motivation. Wanting is sometimes congruent with our needs, but not always. Let’s consider some examples.

Slide 4: Needs, Drives & Motivated Behaviours
Some needs are obvious and universal, like the need for food.
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We NEED energy and nutrients, certainly we can’t live without them, so the DRIVE of prompts a motivated BEHAVIOUR, in this case eating. This trio of need-drive-behaviour is seen in all animals and, in fact, the biological processes that trigger and control hunger are very similar in humans, rats, and mice.
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The need for water is also easily understood in terms biological deficiency; thirst becomes overwhelming if we get severely dehydrated, so it promotes drinking behaviour. However, ALL motivated behaviours don’t fit as neatly into this tidy framework.
Take knowledge for instance.
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Clearly, we humans go to great efforts to acquire knowledge and understand what’s going on around us. Curiosity is a strong motivator in other animals as well, and it drives exploration. BUT, does this fit the definition of a need? You won’t necessarily die from lack of knowledge, so it’s not as critical to survival as food or water. We’ll review several different theories of motivation and consider how well they explain these different types of goal-directed behaviour.

Slide 5: William James & Instinct Theory
One of the earliest thinkers to weigh in on motivation was William James, who is considered to be the father of American psychology. He hypothesized that behaviours are driven by different instincts that help us survive. Instincts are defined as unlearned behaviours shared by members of a species.
Some instincts, like feeding
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are obvious and are common amongst all animals
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Other unlearned behaviours described by James, such as a baby seeking out a nipple for milk
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are also related to survival, as is the mother’s instinct to protect the child. However hunting prey was also considered by some to be an unlearned human instinct, and there was a lot of disagreement between researchers on what behaviours should be included. Furthermore, emerging evidence showed that learning could have a powerful effect on motivated behavior, and instinct theory could not account for this.

Slide 6: Evolution & Natural Selection
James was strongly influenced by Charles Darwin’s theory of evolution through natural selection. At the core of this is the idea that the purpose of any living organism is to perpetuate itself. You’ve likely heard the phrase, survival of the fittest, which is the cornerstone of Darwin’s theory of natural selection. From this perspective, fitness refers to the ability to survive AND reproduce.
Basic needs, such as food, fluids and optimal temperature are often explained from this perspective. If we become deficient in some need, drives can redirect our behaviour towards goals that can keep us alive. Given that certain motivated behaviours are shared by all animals, the evolutionary model suggests that they were naturally selected for in our early ancestors, because they promoted fitness.
So it’s easy to appreciate how James was swayed by Darwin’s theories at the time.

Slide 7: Drive Reduction Model
Another prominent theory related to evolutionary model is the drive reduction model. It extends the evolutionary model and adds explanation about the mechanism of motivation. It states that behaviour is driven by the need to balance physiological systems when depleted and is closely tied to the idea of homeostasis,
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the tendency to maintain balance in biological systems.

Slide 8: Homeostasis & Set Point
According to drive theory HOMEOSTASIS sets up equilibrium around an optimal set point, or fixed setting, of a particular physiological system.
The drive reduction model of motivation is based on the body’s tendency to maintain homeostasis, we’ll consider temperature. This model suggests that there are sensory detectors that monitor the current state, which is compared to the body’s set point,
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which for temperature in humans is about 37 degrees Celsius. If it’s too hot
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then the body kicks in various cooling responses, such as sweating or behaviours like removing clothing or relocating to a cooler place. If it’s too cold,
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then the body activates heating responses, such as shivering or behaviours such as adding a layer of clothing.
This perspective is obviously dependent on set points, and we know the set point for body temperature in humans. But what about other drives such as hunger?
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What is the set point for food? We require many different types of nutrients, but there don’t appear to be simple set points for sugars and fats in the same way there is for temperature, so the drive reduction model can’t fully explain how hunger and feeding work. Another issue with this model is that some strong drives (like sex drive) don’t appear to be driven by physiological set points at all.

Slide 9: The Optimal Arousal Model
The optimal arousal model of motivation argues that humans are motivated to be in situations that are neither too stimulating nor not stimulating enough. Sort of the “Goldilocks principle”, not to boring, not too stimulating, but just right.
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Support for this model is supported by observations of people in the 1950’s who volunteered to undergo SENSORY DEPRIVATION, usually achieved by having them spend long periods of time in a sensory deprivation or ISOLATION tank.
Most volunteers could not remain in sensory deprivation for more than two to three days even if they were paid double. Long-term deprivation led to “pathology of boredom” and sometimes resulted in hallucinations and cognitive impairment. The interpretation from these findings was that the brain will CREATE stimulation if it’s lacking, and is the foundation of the optimal arousal model.

Slide 10: Yerkes-Dodson Law
The Yerkes and Dodson Law is not strictly related to motivation, but it uses the idea of optimal arousal to explain effects on performance.
This law states that moderate levels of arousal lead to optimal performance.
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At low levels of arousal,
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such as during boredom or apathy people show very poor, or even NO performance on a given task. At high levels of arousal such as with states of panic,
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people’s task performance on just about anything is quite bad. There is a sweet spot in the middle where just the right amount of alertness leads to the best task performance.
Yerkes and Dodson also found in their experiments that optimal arousal effects differ with task difficulty. More difficult tasks shift the curve to the left, meaning levels of anxiety are particularly damaging for novices.
Yerkes and Dodson’s research was done over 100 years ago in mice, and although there has been some support from human studies, this phenomenon is not really a law.
Another criticism is that performance IS NOT EQUAL TO MOTIVATION, but motivation and performance often go hand in hand (think back to the last time you wrote an important exam).

Slide 11: Maslow’s Hierarchy of Needs
Finally, we come to Abraham Maslow’s Hierarchical Model of motivation which attempts to explain basic biological needs, such as food and safety as well as needs not directly tied to survival, such as personal achievement. Maslow’s model organizes all of these diverse needs into a hierarchy according to priority, arranged in this pyramid. At the bottom
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are physiological needs, such as the needs for food, water, and adequate body temperature.
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On the next level are security needs, which include the needs for physical security, stability, and safety from threats.
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Next are social needs, including the desire for family, friendship, and belonging to a social group.
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The fourth level in Maslow’s hierarchy of needs is the need for esteem, the need to appreciate oneself and one’s worth.
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And, at the top of the pyramid is self-actualization, the full realization of one’s potential.
This model is useful in that it gives organization to a diverse collection of motivated behaviours. It suggests that basic needs must be met first before progressing up the hierarchy. However, this model doesn’t have a lot of scientific support. Critics of Maslow’s model point out that belongingness in social species such as humans is critical for many physiological needs, and therefore this hierarchy might not be accurate.
However, Maslow’s pyramid attempts to explain motivation based on both needs, at the bottom, and wants at the top.

Slide 12: Theories of Motivation
So there you have it, a messy, complicated, but hopefully interesting introduction to the psychology of motivation.

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Tricky Topic: Hunger

Slide 1: Hunger
Hunger is a fundamental drive, since it keeps us alive. If we weren’t motivated to eat, we’d die after about a week or so. But, our relationship with hunger, feeding and food is quite complex. Even though, from a biological point of view, food is just fuel to keep our bodies working, we don’t treat food as a simple energy source. For example,
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Slide 2: Mmmm
…some (or even all) of these foods might look IRRESISTABLE to you. OR you might be the rare person who doesn’t like popcorn, pizza, or pancakes, so you might choose NOT to eat these foods if offered. Maybe you love pizza, but HATE black olives.
But what if you were REALLY, REALLY, REALLY hungry? Would you eat whatever food is available, even black olives? What influences your decision? It turns out that there are two main types of influences on hunger.
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Slide 3: Influences on Hunger
The first is biology, which is all about meeting energy requirements.
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The second main influence is psychology, which concerns how our experiences, memory, expectations, and thoughts control the types and amounts of food we eat. We’ll start first
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with biological influences. So where are the hunger control centres?

Slide 4: Stomach
Well, one sensible starting place is the stomach, which is hard to see in this illustration with the rest of the internal organs in the way, but it’s located here.
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If you don’t eat for a period of time, you might have noticed your stomach growling. Is that a NECESSARY part of the hunger response? The short answer is no, not really, but let’s look at some of the evidence that supports this conclusion.
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There are sensory nerves that allow the stomach to communicate with the brain, so it seems possible that these might be responsible for signalling when its empty.
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However, if these nerves are cut surgically, individuals still feel hungry and full. Some other evidence comes from research on people who have undergone gastric bypass, where the majority of the stomach is removed, and these individuals still have feelings of hunger.

Slide 5: Blood
Things circulating in the bloodstream are important signals to our energy status. We absorb three main types of energy sources from the food we eat fat, protein, and carbohydrates. Carbs are a readily available source of food energy since they can be broken down fairly easily into simple sugars.
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One bloodborne substance that appears to be important in hunger is glucose.
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When we go without food for a long period of time, our blood glucose levels drop, and this is detected by special areas in the brain involved in hunger.

Slide 6: The Hungry Brain
The hypothalamus, which is located right about here in a human brain, has an important role in controlling hunger. Since hunger is very similar in humans and other animals, a lot of what we know about the hypothalamus and feeding is from studies with rats
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The hypothalamus is located roughly here
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In real life, a rat brain looks like this from the side view,
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but if we flip the brain so that we’re looking up at it from underneath,
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the hypothalamus is located in this region.
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If we were to take a section through this part of the brain and lay it flat so we can see the structures inside…
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Slide 7: Hypothalamic Feeding Areas
…it looks like this. The hypothalamus is down here
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at the bottom of the brain.
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This darkly coloured region is a collection of neurons that make up the ventromedial hypothalamus,
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which reduces feeding by promoting feelings of satiety, in other words feeling full. This part of the brain stimulates the SYMPATHETIC NERVOUS SYSTEM, responsible for FIGHT or FLIGHT functions, and destruction of this area leads to overeating and weight gain.
The region here at the sides of the is called the LATERAL HYPOTHALAMUS
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and it is involved in promoting feeding. When this area is stimulated, animals IMMEDIATELY feed, even if they’ve already eaten.

Slide 8: Hormones/Neurochemicals
It turns out that there are a bunch of chemical messengers that are involved in hunger and satiety (inhibiting feeding). These all communicate, usually directly, with the hypothalamic areas just described. Neuropeptide Y is one of the most potent appetite stimulators ever discovered, since if it’s introduced into the brain of a lab rat, it will immediately eat, even if it has just eaten a meal. Orexin, ghrelin, melanin, and the endocannabinoids (which bind to the same receptors as marijuana) are all appetite stimulators
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that promote feeding.
On the other hand, there are also a ton of chemical messengers that reduce feeding
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Insulin (which is released when we eat carbohydrates) acts on the hypothalamus to inhibit feeding. Leptin, released from fat cells also acts on the hypothalamus to reduce food intake. Peptide YY and cholecystokinin (known by its abbreviation, CCK) are chemical messengers released from the gut organs in response to food intake, and they reduce feeding as well.
So clearly there are a lot of checks and balances on feelings of hunger and satiety, so it makes you wonder why anyone would over OR under eat. There must be something more to this story.

Slide 9: Influences on Hunger
Even though our biology is wired for us to eat when we require energy, and stop when we have enough, our experiences have a huge effect on feeding. So let’s look at some of the psychological influences on feeding.

Slide 10: Food Preferences
Here’s a quick test. Which would you prefer to eat, a banana from the bunch on the left or the right? Most people will choose the nice, clean yellow bananas. Why? They look much fresher and probably taste better. The bananas on the right are probably all soft and squishy. All of these bananas shown here are perfectly fine to eat, I know because I ate them. However, we have a bias to fresh-looking foods. It’s not an accident that we eat very few blue-coloured foods, since moldy food is blue.
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Let’s return to some of the foods I showed earlier. Do these appeal to you more than these?
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How hungry would you have to be to eat raw oysters? What about brussel sprouts? Black licorice? These are amongst the top 25 most hated foods, according to a quick search on Google. What is it about these foods that turns people off? They all have nutritional value, so can fulfill biological needs for energy. Is it because they are unusual? Or do they actually taste bad?
A HUGE factor in food preference is prior exposure in our family or culture, and an enormous impact on what we choose to eat.

Slide 11: Conditioned Hunger
As Pavlov’s research on learning showed, signals outside the body can have a strong impact on the digestive system. He taught dogs to drool in response to a bell by pairing the sound of the bell with meat, which dogs instinctively drool for.
Cues associated with food through classical conditioning can trigger hunger in people too.
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If you habitually check the time to see when to break for lunch, as millions of people do every day, the clock face showing that’s it’s lunch time becomes like Pavlov’s bell, it becomes a PREDICTOR of food availability
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and triggers feeling of hunger
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Using external cues to tell us when we’re full can be problematic, since internal cues are much better indicators of energy need. How do you know when YOU’RE hungry or full? Do you listen to your body or look at your plate? The “finish your plate” rule is certainly a good idea to prevent food wastage, but some believe that it might promote overeating and obesity.
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Slide 12: Expectancy
Research by Brian Wansink’s laboratory suggests that we become so used to using external cues that we ignore our internal signals. In other words, we eat with our eyes, not with our stomachs. Wansink did a clever experiment where he gave two groups of participants a bowl of tomato soup and told them to enjoy as much as they wanted.
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Half of the participants ate from a special refilling bowl, which was connected to a heated container of soup hidden from view. So their eyes were tricked into thinking they were eating a normal bowl of soup. Afterwards, both groups gave very similar estimates of how much they thought they ate, but when this was compared to how much they actually ate,
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those in the refilling soup group consumed much more than the controls.

Slide 13: Hunger
Therefore hunger is controlled by BOTH biological and psychological factors. Although our digestive and nervous systems give us plenty of signals about when we should eat, AND when we should stop, our personal histories and experiences can override these signals. The interplay between biology and psychology are a huge part of maintaining energy needs and body weight.

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Tricky Topic: Theories of Emotion

Slide 1: Theories of Emotion
Feelings are very powerful experiences, and there has been a lot of argument and disagreement about HOW they’re produced. Where do subjective feelings come from? There are four prominent theories that have tried to explain this.

Slide 2: James-Lange Somatic Theory
First is the James-Lange Somatic theory, named after William James and Carl Lange. The term SOMATIC means body, which is the starting point of the creation of feelings according to this view. Basically the idea is that we experience emotion internally IN RESPONSE TO physiological changes. Keep in mind that this should happen for positive emotions as well, but it’s much easier to demonstrate with negative emotions.
Say you see something frightening, like approaching zombies. The James-Lange theory suggests that FIRST,
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your body reacts by pumping up heart rate and respiration and other physiological changes, and this gets detected by the brain and creates a subjective emotional experience,
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in other words, feelings of fear. This theory is somewhat counter-intuitive, because it places FEELINGS last as a response. This theory is supported by the fact that our bodily responses can FEEDBACK to our experiences. In fact, people report feeling happier when holding a pen in their teeth (which activates smiling muscles) compared to holding a pen in their lips, (which activates frowning muscles). Give it a try and see how YOU feel.

Slide 3: Cannon-Bard Theory
The Cannon–Bard theory, named after Walter Cannon and Phillip Bard, states that feelings occur independent of emotional expression, in other words, there is no correlation with physiological state and emotional responses happen in parallel. Support for this theory comes from research showing that there are multiple parallel pathways in the brain that respond to emotional triggers,
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and that the pathway through the thalamus leads to a whole host of physical and physiological changes,
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while the pathway through the cortex is important for the subjective emotional experience.

Slide 4: Two-Factor Theory of Emotion
The two-factor theory of Schacter & Singer states that our conscious experience of emotion is determined by both an awareness of what’s happening in the body
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AND a cognitive appraisal of the situation.
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In other words, we make a decision about which emotion we’re experiencing based upon the explanation that best fits the circumstance.
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So, if you see approaching zombies you don’t just robotically respond with fear, rather you look at what’s happening in your body AND also make some sense from what’s happening in the situation. Sometimes you might not be all that afraid of zombies.
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For example, if you saw approaching zombies on your favourite zombie series, you might feel your heart racing, BUT this would also paired with an appraisal of the situation. In my case, because I’m a big fan of the zombie genre, this would lead me to feel very happy, rather than terrified (which is how I’d feel if I ever saw the zombies in real life).

Slide 5: Cognitive-Meditational Model
In contrast to Schacter and Singer’s two-factor theory, Lazarus proposed the cognitive-mediational theory which places cognitive appraisal as the FIRST step in the emotion process. Once the individual makes an appraisal of the situation and ability to cope
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this can then trigger all of the emotional responses.
This theory is supported by the fact that different people respond to the same antecedent stimulus (in this case zombies) with different reactions. Lazarus showed that the appraisal process has a big impact on whether a stimulus triggers and emotion and how intense it will be.

Slide 6: Theories of Emotion
Although neither of these theories explains all aspects of subjective emotions, each has its strengths and weaknesses so modern views of emotion incorporate evidence from all of them

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Tricky Topic: The Emotional Response

Slide 1: The Emotional Response
For many, many years researchers argued over what best defines what an emotion.
Are facial expressions the most important response to an emotional event – certainly they change with emotional states. What about the feelings emotions trigger inside, are those the most relevant responses? Or is it instead the physical changes in the body, like a racing heart, that tell us about emotions. Researchers came together on this fairly recently and now recognize that we can best understand emotions by considering the MANY responses that accompany them. So the modern view is to leave nothing out and to view emotion as a process.

Slide 2: The Emotion Process
So let’s take a quick look at the EMOTION PROCESS, since emotional responses are the end result.
First there’s some sort of antecedent event, something that TRIGGERS the emotion. There are lots of examples, for me a seeing a puppy or kittens automatically makes me happy. So these stimuli are ANTECEDENT to the emotion of happiness for me. Other antecedent events, such as an upcoming exam might invoke feelings of panic or anxiety for some people, others get totally freaked by spiders. These stimuli are antecedent to the emotion of fear.
What all of these antecedent events all have in common is that they prompt us to make an appraisal
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which is the next step in the emotion process where we make sense of the thing we have encountered.
Depending on the results of the appraisal there is an emotional response
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which is actually a collection of responses by the body and brain. These can be categorized as PHYSIOLOGICAL CHANGES, BEHAVIOURAL/EXPRESSIVE CHANGES, AND SUBJECTIVE CHANGES, which will be the focus of this tricky topic.

Slide 3: Three Response Components
These three changes represent the body’s response to an emotional event. They each have a different function to help us deal with emotional situations.
Physiological changes are changes in the body that come with emotions like changes in heart rate.
Behavioural-expressive changes involve observable behavioural responses, the most obvious of these in humans are facial expressions.
Subjective emotional experiences are what we call FEELINGS

Slide 4: Physiological Changes
Physiological changes are mainly controlled by the AUTONOMIC NERVOUS SYSTEM which has two divisions, the sympathetic
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also called fight or flight and whose neurons exit from the middle of the spinal cord
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and the parasympathetic
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also known as rest and digest and originates from cranial nerves and the posterior spinal cord
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Fight or flight responses get activated with INTENSE emotions, like terror or excitement. There are a whole host of autonomic changes, but the ones we notice most often are racing heart and increases in respiration.
The rest and digest responses are activated when we’re relaxed and content, and these are less noticeable because heart rate and respiration relax.
All of these responses are involuntary so we don’t have a lot of conscious control over them.

Slide 5: Behavioural-Expressive Changes
The behavioural-expressive changes involve observable body movements, and of course what we humans notice most is what happens on the face. We’re are wired respond to faces; newborn babies even mimic the facial expressions of adults.
But how can we study these facial expressions, how do psychologists manipulate and measure them?
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The Facial Action Coding System (FACS) is a widely used method developed by emotion research Paul Ekman. He had volunteers move different combinations of facial muscles, and had coders score all observable muscular movements possible on the human face.
He found that certain combinations of muscles were interpreted as specific emotions by others who observed them. It’s widely accepted that these behavioural changes in the face are important for communicating emotional states, and cross-cultural research indicates this is universal.

Slide 6: Emotional Communication
Some other interesting research on the facial action coding system has revealed that true and fake emotions are expressed differently on the face. Which smile looks genuine, the one on the left or the one on the right? Most people would choose the one on the left. This smile is called a Duchenne smile,
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after the French anatomist who first described it. Why was an anatomist interested in smiling? Well. it turns out that genuine happy smiles involve contracting not only the muscles of the mouth,
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but also the band of muscles that surround the eye.

Slide 7: Emotional Suppression
Because facial expressions are used to display emotions to others, sometimes we suppress them when we want to conceal them. The term poker face refers to a blank expression that can’t be read by others. We have much more control over behavioural emotional responses than physiological changes.

Slide 8: Subjective Changes
Subjective changes are internal, personal responses and are what we typically refer to as FEELINGS.
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Each emotion creates a unique feeling – anger FEELS different than happiness. In fact, our internal experiences help distinguish different emotions. For example, both fear AND anger increase heart rate, but they are experienced very differently and triggered by different antecedent events.
The subjective nature of feelings means that the only way that we can measure them is to ask people, using a self-report.
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So, this aspect of emotion can really only be studied in individuals with verbal ability.

Slide 9: Measuring Emotional Responses
Given the diversity of reactions to emotional events, measuring emotional responses comprehensively requires a large toolkit. Physiological changes are usually detected by measuring some aspect of autonomic nervous system function associated with arousal,
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such as heart rate, blood pressure, and respiration. The polygraph or “lie detector” test is based on the assumption
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that telling a lie creates anxiety or tension. Although the liar might try to hide this tension by altering facial expressions and movements, it’s difficult to control the what’s happening inside the body.
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Behavioural responses can be measured by observing an individual under different emotional conditions, and if this is done in humans, facial expressions are the easiest behaviour to detect. Although facial expressions of emotion appear to be universal across all humans, we can easily exaggerate or suppress our emotional displays, and therefore they might not be as accurate a predictor of emotions compared to physiological responses.
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Subjective feelings are measured by self-report, usually with some sort of rating scale for intensity of different emotions. One issue with this is that non-verbal individuals,
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such as babies and animals, cannot complete self-reports so we infer how they’re feeling by other behaviours.

Slide 10: The Emotional Response
So the emotional response is multi-faceted and complex, and still not completely understood.

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Tricky Topic: Freud’s Theory of Personality

Slide 1: Freud’s Theory of Personality
This Tricky Topic will focus on Freud’s theories and evaluate the useful, and not-so-useful contributions to the study of personality. Before we delve into Freud, let’s review what’s meant by this term.

Slide 2: Personality
Psychologists define personality as unique and enduring set of behaviours, thoughts, feelings, and motives that characterize an individual. So personality is what makes us US and not someone else. According to this definition,
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personality stays relatively stable over time and across different situations. This is really useful to us; we use personality information all the time because it allows us to predict what people like and dislike, and how they’ll behave under certain circumstances. When we’re buying gifts, planning a party, or choosing a romantic partner, what we know about others’ personalities guides our decisions.
Let’s look at an example.
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Both of these kids shown here on the right were just told by their parents that they are moving across the country and will have to go to a new school and make new friends. Which girl will feel most distressed by this? Most of us would choose the girl on the top. And if these images are indeed true reflections of their personalities, we’d probably be right.
So where does Freud fit into all of this? His perspective on personality is closely tied to his approach to treating mental illness, which is what he’s most famous for.

Slide 3: Freud’s Legacy
Freud’s biggest legacy is his creation of the field of psychoanalysis, a strategy of using *talk therapy* as a way to modify behaviour. Freud’s name for many people conjures up an image like this one:
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Someone lying on an armless couch, revealing their innermost desires to a therapist who sits in the background, taking notes and making interpretations. Although Freud’s exact therapeutic techniques aren’t widely used today, this treatment approach is one of the foundations of modern clinical psychology.
Freud’s approach to treatment rested heavily on the assumption that a big part of who we are comes from our early life experiences,
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which can result in a unique and enduring set of behaviours, thoughts, feelings, and motives that characterize an individual; keep in mind that this is our working definition of personality. So let’s look at Freud in more detail.

Slide 4: Sigmund Freud (1856-1939)
Sigmund Freud was an Austrian neurologist and one of the best known figures in modern psychology.
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Freud’s clinical practice was heavily influenced by a fellowship to study with French neurologist Jean-Martin Charcot in 1885. Charcot was exploring hypnosis as a way to treat patients with what was known at the time as hysteria, a disorder of physical complaints with no known cause.
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From this Freud became interested in the power of the unconscious mind, and he developed techniques, including dream analysis and free association to unlock the mind’s unconscious motives.

Slide 5: Freud’s Idea of the Mind
The foundation of Freud’s ideas about personality and mental illness was his representation of how the mind is structured.
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He stated that the mind has three layers of consciousness, the conscious (which is whatever is going on in your mind right now), the preconscious (which are things that can be called into conscious thought), and the unconscious mind (which is all the stuff that sits outside conscious awareness, but can have powerful effects on thought and behaviour). Freud believed the unconscious mind was a largest component of consciousness.
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In addition to these difference levels of consciousness, Freud also hypothesized that there are three distinct components or PROVINCES
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that control impulses that arise from the unconscious. According to Freud,
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the ID is the first to develop and is the seat of impulse and desire. It operates on the pleasure principle and guides behaviour to self-gratification.
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The EGO, is the next to develop, around the 1st year of life and operates on the reality principle, and attempts to make realistic attempts to obtain self-gratification. Unlike the ID, the ego has direct contact with the outside world.
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The last province to develop is the SUPEREGO, which develops around ages 2 or 3 and operates on the moral principle and evaluates our actions in terms of right or wrong. According the Freud, the superego is in constant battle with the ID to try and control unconscious urges and desires.
So how does this influence personality?

Slide 6: Individual Differences
According to Freud, in a psychologically healthy person
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the EGO strikes a balance between the urges of the ID and the control exerted by the SUPEREGO. In contrast,
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an overly controlling person has a relatively large SUPEREGO that represses the urges of the ID. On the other hand, in someone who is an overly impulsive person,
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the ID predominates so the individual seeks pleasure without the right balance of moral guidance.
Freud hypothesized that dealing with the impulses of the id can cause problems, so…

Slide 7: Dealing with the ID
…he theorized that mind uses DEFENCE MECHANISMS to protect itself from the threat of anxiety-promoting thoughts or impulses that arise from the id. Freud stated that these defence mechanisms
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OPERATE UNCONSCIOUSLY and DENY or DISTORT REALITY in some way.

Slide 8: Defence Mechanisms (Anna Freud)
Although these were first proposed by Sigmund Freud, they were fleshed out by his daughter, Anna.
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The best described of the defence mechanisms is repression,
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which is keeping unpleasant thoughts, feelings, or impulses out of consciousness awareness.
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Reaction formation is turning an unpleasant idea, feeling, or impulse into its opposite.
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Projection is described as denying or repressing ideas, feelings, or impulses and projecting them on to others.
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Sublimation is expressing socially unacceptable impulses into a socially acceptable way and
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fixation is being preoccupied with an earlier stage in development.
These defence mechanisms are very popular since it’s quite easy to come up with examples. Take reaction formation, for instance. Let’s say someone is uncomfortable about the fact that they might have homosexual tendencies (maybe because of way they were raised), so they deal with this conflict by flipping it around and outwardly expressing homophobia. On the surface this appears to make sense, but these defence mechanisms are very difficult to test since they deal with thoughts that are unconscious AND subjective, so they’re VERY DIFFICULT TO MEASURE. Furthermore, there’s no solid evidence that the id, or other provinces, exist in the mind, so theories that grow from this assumption are not well supported.

Slide 9: Psychosexual Stage Theory
Probably one of the most controversial ideas of Freud’s is his PSYCHOSEXUAL STAGE THEORY, summarized in this table. Basically Freud hypothesized that personality develops in stages throughout early life, and that each age is concerned with pleasure-seeking from a particular area of the body. The first stage, according to this theory, is the
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oral stage that occurs between birth and 18 months. Children at this age spend a lot of time putting things in their mouth and Freud believed that fixations resulted in excessive behaviours in adulthood that involve the mouth, like smoking and sarcasm.
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The ANAL stage is next from the ages of 18-36 months, where children spend a lot of time learning how to potty train; fixations on the anal region at this stage results in obsessive and compulsive cleaning behaviours (that’s where the term anal retentive comes from). The other stages are equally bizarre, but more importantly, from a scientific point of view they’re not grounded in sufficient evidence.
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In fact, since these theories were developed, there has been absolutely NO support for this view of personality. It did open the door however, for the idea that early life experiences can affect thought and behaviour in adulthood.

Slide 10: Summary
So to summarize, Freud had a powerful influence not just on the study of personality, but also clinical psychology. If we look at the evidence that has amassed since Freud proposed these theories,
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there’s certainly evidence for a powerful role of unconscious thought processes, which has been embraced by cognitive psychologists and rebranded as implicit thinking. Also
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the role of early life experiences in adult behaviour has been supported by research in
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behavioural neuroscience with the field of epigenetics which has revealed long-term changes in gene expression as a result of early life events
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This idea has also been influential in clinical psychology with studies of the effect of early life trauma. However,
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the psychosexual stages of development theory, which is the theory most directly tied to ideas of personality, have not been supported with evidence.

Slide 11: Freud’s Theory of Personality
Sigmund Freud is arguably psychology’s best known AND most controversial figure, but his ideas have contributed more to literature than they have to the study of personality. He introduced some ideas that did NOT withstand later scientific scrutiny, but he did make some important contributions to our understanding of the influence of early life events and the role of the unconscious.

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Tricky Topic: The Big Five

Slide 1: The Big Five
The Big Five model has been the most influential in guiding modern research on personality; most studies of personality use measurement tools based on its assumptions. Also called the FIVE FACTOR MODEL, it explains personality in terms of five broad categories of traits. This might seem limited to measure something as widely diverse as personality, so we’ll first look at how this idea developed.

Slide 2: What Makes up Personality
Early influential views of personality; psychoanalytic, humanistic, and social-cognitive emphasized the causes of personality but the tools to measure it were vague or lacking, which makes these theories tricky to research scientifically. One attempt to remedy this is to define personality in concrete terms so it can be measured. One way to do this is to look at the building blocks of personality.

Slide 3: Trait Theories
Trait theories of personality differed from others n that there was a much greater emphasis placed on measurement. This approach was strongly guided by the LEXICAL HYPOTHESIS
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which suggests that we can turn to language to determine what makes up personality.
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The most ambitious attempt to apply the lexical approach was carried out in the 1930s by Gordon Allport and Henry Odbert using a good, old-fashioned dictionary. They started off looking for adjectives that described a person and got almost 18000! So, they took out words that dealt with short term moods or emotions, and that left just over 4000. They eventually whittled it down to under 10, reasoning that most people can be described with 10 traits, but there wasn’t any HARD scientific basis for this.
However, this was an important start and got others thinking about how to whittle down the many traits we have words for into a manageable list.

Slide 4: Let’s Try It!
So, let’s try the lexical approach to personality. Pause this video and go get a piece of paper and something to write with. Ready? I’m going to give you 30 seconds to write down some adjectives that can be used to describe someone’s personality, in no particular order, just write down as many as you can. Ready? Go.
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Ok, let’s compare our notes
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So here are some items from my list. Did you have any items similar to these? You can group related words into categories
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With these words, I came up with four clumps, and what I noticed about them is that some of my clumps were on opposite ends of a spectrum,
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with some being high and others low for a particular trait.
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This approach is conceptually easy to do, but very cumbersome given the huge numbers of descriptive words. Keep in mind that we only took 30 seconds to devise our lists. So, thankfully we have nerds called statisticians who love to analyze large sets of data, so they had people rate themselves on a scale for lots of different traits and crunched the numbers using a statistical technique called factor analysis
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to reveal FIVE clusters or factors capturing descriptive personality words. These can be remembered easily using the mnemonic OCEAN,
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for Openness, Conscientiousness, Extraversion, Agreeableness, and Neuroticism. Let’s look at these factors in a bit more detail.

Slide 5: The Big Five
Keep in mind that each of the Big Five traits is made up several smaller building blocks, but descriptions of traits at the high and low ends of each one is outlined here.
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Openness describes how interested someone is in new experiences and ideas and how imaginative, original, and curious they are.
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Conscientiousness refers to how planned, organized, orderly, hard-working, controlled, punctual and ambitious someone is.
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Extraversion refers to how sociable, active, outgoing, and confident someone is.
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Agreeableness refers to how friendly, trusting, generous, and good-natured someone is.
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Neuroticism refers to how anxious, tense, emotional, and high strung someone is.
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Let’s look at one of these in more detail.

Slide 6: Dimensional Measurement of Extraversion
So, when measuring where someone would fall on one of these dimensions, researchers ask lots of questions and get people to rate how much they agree with statements describing themselves. These three statements here measure the dimension of extraversion, which I pulled from a larger Big Five questionnaire: READ THEM. Someone who is private and introverted might answer these questions like this
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Someone who is really extraverted might answer these same questions like this
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However, most people aren’t EITHER introverted OR extraverted, most of us would likely answer the questions somewhere in the middle of the range of this dimension.
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By looking at each dimension of the Big Five, these self-reports of personality can be quantified.

Slide 7: The Big Five in the Population
If we look at people’s scores for extraversion in a large population, there are a few people at the extremes,
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but most of us are in the middle. The same is true for neuroticism, which refers to emotional instability
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Some people are low in neuroticism, while others are high on this trait, but most of us fall somewhere in the middle. One interesting thing about the Big Five dimensions is that, statistically, they all appear to fall along this NORMAL DISTRIBUTION.
The Big Five dimensions are more of a taxonomy, or categorization scheme, than a theory. This model has been criticized because it mainly DESCRIBES but does not explain personality. However, the model certainly allows people to test theories that DO try and explain personality, since scores on these traits are associated with particular behaviours. Questionnaires that assess the big five traits SHOULD be associated with behaviours relevant to that trait.

Slide 8: Big Five in Social Media
This study surveyed over 66 000 Facebook users who completed the revised NEO personality inventory, called the NEO-PI-R for short, and compared this to words in users’ status updates.
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These word clouds were created for participants who scored high on extraversion on the left and those that scored low on this trait on the right. The size of the font shows the strength of the correlation between use of the word and extraversion scores
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while the colour coding shows the relative frequency of the word use, with red indicating higher use
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If you take a moment to look at the word clouds, it’s clear that extraversion is associated with different language in status updates compared to introversion. For instance, for intraversion note use of words like
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don’t, didn’t, doesn’t, and isn’t, whereas these words are rare in the extroverts’ statuses. The researchers suggest that the use if these negative action words align with differences in the need for stimulation at the extremes of this trait. Given the large sample size and the fact that it was drawn from a wide sample of Facebook users, this provides support that the Big Five traits are capturing a meaningful representation of personality.

Slide 9: The Big Five
So the Big Five Model has given us a reliable way of measuring personality and is much less subjective than the methods first developed by Freud, which relied on interpretation of the researcher. It also appears to capture many of the aspects of personality, and so the BIG FIVE model remains the most influential in modern research on personality.

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Tricky Topic: Fundamental Attribution Error

Slide 1: Fundamental Attribution Error
How we attribute the causes of others’ behaviour colours how we perceive and ultimately judge them. It turns out that when trying to figure out others’ intentions, we have tendency to process information in a biased way, and SOMETIMES leads us to make mistakes. This is sooo common that it’s called the FUNDAMAENTAL ATTRIBUTION ERROR, which will be the focus of this Tricky Topic.

Slide 2: Attributions
So what are attributions? Quite simply, they are explanations we make for causes of behaviour. These are also sometimes called causal inferences.

Slide 3: Example
So here’s an example. You’re bombing along a side street on your bicycle, feeling the wind in your hair and, ALL OF A SUDDEN out of nowhere some guy comes racing along and cuts you off….
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…forcing you to slam on your brakes and almost fall head over heels. How would you feel? Scared, probably. Angry, definitely. What’s your gut instinct about this guy?
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Do you explain his behaviour like this,
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“that guy’s a total jerk”, how did he get his license? If so, you’ve made a dispositional or internal attribution for his reckless behaviour. Or rather, do you explain his behaviour by looking at factors outside of his personality,
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considering that he might have an emergency situation that requires him to drive fast and furious to help someone. If this is where your mind takes you, you’ve made a situational or external attribution.

Slide 4: Attributions & Social Judgements
So why does this matter? It matters a LOT because how we make attributions is a big part of what we use to make judgments. So let’s look at the impact of making dispositional and situational attributions when explaining the causes of positive and negative behaviours. If someone does something positive and we figure it’s due to something internal to that person,
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we’re probably going to like that person and think they’re kind or generous. On the other hand, if someone does something negative and we attribute that to something internal to that person,
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we’re probably NOT going to like that person very much at all. We might think they’re mean or cruel or a jerk. If someone does something positive however, and we think the cause of this apparently kind behaviour is due to the situation,
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we probably won’t like this person very much. We’ll think that they did this nice thing just to get ahead or for selfish reasons. And lastly, if someone does something negative that we this was caused by the situation,
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we might not feel so judgy toward that person. Even though we might not admire that person, we probably won’t feel really negative about them.
So when do we use dispositional and situational attributions?

Slide 5: Self-Serving Bias
Now when it comes to our own behaviour, we usually explain it in a way that makes us look good and feel better about ourselves.
What if YOU were the person driving like a jerk? How would you explain the cause of your own negative behaviour?
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Are you likely to use a dispositional attribution and admit we’re being a jerk? Or rather
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we more likely to use a situational attribution and blame it on our circumstances? It turns out the most of the time we use the self-serving bias when it comes to our own behaviour.

Slide 6: Attributions & the Self-Serving Bias
So if we return to this table
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we’re more likely to use dispositional attributions when we’re explaining our own POSITIVE behaviour (I donated to that charity because I’m a nice person) but situational attributions for our own NEGATIVE behaviour (I cut that cyclist off because I had an unusual situation).
So what do we do when we’re explaining others’ behaviour?

Slide 7: Fundamental Attribution Error
Something very different happens when we evaluate others’ behaviour. We have a tendency to rely on dispositional rather than situational explanations.
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In other words, when viewing others’ behaviour,
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we’re likely to pay most attention to the actor and ignore the stage. This tendency is SOO strong, that‘s referred to as FUNDAMENTAL and because it often leads us to make mistakes, therefore this is referred to as the fundamental attribution error.
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So our biases can influence how we evaluate others, so keep this in mind the next time you give credit, or blame, to someone else.

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Tricky Topic: Cognitive Dissonance

Slide 1: Cognitive Dissonance
One of the most surprising and powerful forces for attitude change is a phenomenon called cognitive dissonance, first proposed by psychologist Leon Festinger in the late 1950’s.

Slide 2: The Need for Internal Order
Although we’re not often aware of it, we humans have a strong need for internal order and consistency. We like to see ourselves as sensible, rational, and reasonable people. But when we’re faced with evidence that contradicts this, it makes us feel uncomfortable, and we’ll go to great lengths to reduce or avoid this feeling of discomfort. This was the focus of a classic experiment done by Festinger and Carlsmith in the 1950s. They wanted to see what would happen when they tricked people into doing something that made them feel uncomfortable about their self-concept as a reasonable person.

Slide 3: Festinger & Carlsmith, 1959
What they did was set up a situation where people’s opinions didn’t match their behaviour. They had 60 participants complete an hour of tedious boring tasks. One of the tasks went like this:
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Participants were given a tray and 12 wooden spools. They were instructed to place the spools on the tray, take them off, and then put them on again. They were told this was a PERFORMANCE TASK, but in fact it was designed to be boring and tedious for the next part of the study. The participants were randomly assigned into three groups
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with different instructions: the control participants were business as usual, but the two experimental groups were asked if they’d be willing to help out with the next participant because the regular research assistant called in sick. Their job was to go into another room and tell a new participant (who was really a confederate of the researcher) that the task was actually really fun
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so they basically tricked them into telling a bald-faced lie. The $1 group were hired for the small sum of $1 to do this, whereas the $20 group got a whopping 20 bucks, which was a lot of money back in 1959.
Then all groups were asked to rate their own enjoyment of the task (CLICK) on a scale from -5 (dull and boring) to +5 (interesting and enjoyable).
So how much did the three groups of participants ACTUALLY enjoy the task?
Think about that for a minute and make a prediction.

Slide 4: Results
The controls didn’t lie, so they gave their true opinion of the task, and rated it slightly negatively, so this can be considered the baseline rating for the boring task. The interesting results are ratings by those who lied and said it was fun.
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Those that only got $1 for doing so, actually enjoyed the task, and on average gave it a positive rating. On the other hand
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the $20 group rated it close to zero, very similar to the controls.
At this point you might be thinking, wait a minute, why didn’t the $20 group report the most enjoyment, after all, they got a lot of money! According to Festinger, these participants already HAD a fantastic reason for lying, they got twenty bucks! They didn’t need to feel cognitively uncomfortable about lying because they had an awesome (but slightly unethical) reason for doing so.
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It was the $1 group who likely felt uncomfortable about lying, since they didn’t really have a good reason for it.

Slide 5: Cognitive Dissonance
This feeling of mental discomfort that happens when we’re faced inconsistencies in behaviours, thoughts, feelings, or values was coined COGNITIVE DISSONANCE by Festinger. Cognitive dissonance is not any type of discomfort, it’s a cognitive tension that arises when we hold two (or more) contradictory beliefs, or if we behave in a way that that contradicts our beliefs.
According to this theory, when we’re faced with cognitive dissonance, we can use one of three strategies to try and reduce it. We can
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1. Change the behaviour,
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2. change thinking to justify the behavour, or
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3. add a new way of thinking that IS consistent.
Festinger’s participants in the $1 condition probably used the 2nd strategy, they had to come up with a good REASON for telling a lie.

Slide 6: Cognitive Dissonance & Smoking
Let’s take smoking as an example. Everyone knows that smoking’s bad for you, especially with the enormous warnings on cigarette packs. Canada actually has some of the most graphic warning labels, and tobacco manufacturers are required to display these on every pack. So why do people smoke in the face of this overwhelming evidence? As a former smoker, I can tell you one reason is that it’s REALLY hard to quit. So what goes on in the minds of smokers? They engage in a behaviour, sometimes 10 or 20 times a day that they KNOW is bad for them. This likely creates feelings of cognitive dissonance and as shown by research from Festinger and others, we do all sorts of things to make that feeling go away. Here are some strategies that smokers might use.
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They might change the behaviour and quit, which is the point of the warnings on the packages, in fact cigarette sales declined a bit after the warnings were introduced. BUT it’s hard to quit so not everyone is capable or willing to do this. So,
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another way to deal with cognitive dissonance is to change the cognition surrounding the harms of smoking. Sometimes people cherry pick an example, like “My Uncle Ollie has been smoking since he was 10 and now he’s 80 and healthy as a horse.
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Another way to deal with cognitive dissonance is to keep the original thinking (smoking is harmful) but to add a new cognition like, sure smoking is bad, but it helps me deal with stress and stress is MUCH worse for my health.
What this example shows is that sometimes it’s easier to change the attitudes than it is to change the behaviour.

Slide 7: Dissonance & Attitude Change
So next time you’re faced with a situation when what’s in your mind doesn’t match your behaviour, take a minute to think whether you’re changing your attitudes just to avoid feeling mental discomfort. You might benefit from taking a step back and determining if you’re making the right decision.

Slide 8: Cognitive Dissonance
So in a nutshell, that’s cognitive dissonance, one of the most peculiar but powerful forces for attitude change.

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Tricky Topic: Informational and Normative Influences

Slide 1: Informational & Normative Influences
Before talking about informational and normative influences, let’s first talk a little about conformity. Let’s consider a couple of examples.

Slide 2: What Would You Do?
Say you’re sitting in a classroom, listening to a lecture on statistics. All of a sudden, an alarm goes off
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You’re not sure if this is the real thing, so what should you do?
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In response to the alarm, everyone else in the class, including the lecturer, quickly heads out of the emergency door. What would YOU do in this situation? Do you stay put or do you follow?
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Here’s another situation. You’re sitting in the audience at a concert you’re not enjoying all that much. You went along with your friends because they talked you into it, but you’re not really digging it. Once the last song is done, the audience rises for a standing ovation
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What do YOU do? Do you stay seated or do you stand up and clap with everybody else?

Slide 3: Conformity
IF in either of these situations you do what others are doing, you are conforming. Conformity is the tendency to adjust behaviour to what others are doing or to adhere to cultural norms.
There are two main reasons why people conform.

Slide 4: Reasons for Conformity
Sometimes we conform because others are a valuable source of information and appear to know what we’re supposed to do. This is called INFORMATIONAL SOCIAL INFLUENCE and it’s basically following the crowd because they’re right.
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This is what makes us follow others in the first situation when the fire alarm went off.

The other reason we follow others is because we want to be accepted and follow social rules. This is called normative social influence and is driven by the desire to be liked
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or at the very least, not to stand out. This is likely what makes us join in a standing ovation, even if we weren’t impressed by the performance.
In the 1950’s Solomon Asch set out to investigate WHY people conform. He designed a simple yet clever experiment to test the power of group pressure.

Slide 5: Solomon Asch’s Study
He told participants they’d be doing a perceptual task judging the length of lines, as shown here. They had to match a standard line (shown on the left), to one of three comparison lines shown on the right. This is a pretty simple task with a glaringly obvious answer, but Asch rigged it so that this was done in a group of 6-9 confederates
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shown in black, and one actual participant, shown in red. There were several trials and everyone gave their answers out loud, which enabled Asch to manipulate group pressure.
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On some trials, the confederates were instructed to give the right answer.
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On other trials, the majority gave the wrong answer
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Asch referred to these as *critical* trials. The actual participant was always one of the last to respond, so what did he do?
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Asch’s results showed that the minority participant (guy) was often swayed by a unanimous, but WRONG majority.

Slide 6: Results
Let’s have a look at how the minority participants did compared to controls, who did the line length judgements alone.
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Only 5% made mistakes when doing the task on their own, while
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76% made mistakes AT LEAST ONCE, when they did this task out loud with a group.
Now, knowing the % of people who caved in to the group doesn’t really tell us how OFTEN they did it. It turns out that some of those who WERE swayed by the group made errors on lots of trials and others only once or twice. If we look at it as a percentage of the trials where errors were made,
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participants on their own only made mistakes on 0.7% of the trials,
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while in a group mistakes were made 37% of the time.
So, clearly, Asch showed that MANY people will be swayed by the group SOME of the time, even if they’re clearly wrong. But was this because of INFORMATIONAL or NORMATIVE influences? It’s difficult to tell from these two conditions alone, but Asch added another condition to address this question.

Slide 7: Solomon Asch’s Study
In this condition, after hearing the responses of the majority, our participant reported their answers in writing rather than out loud. That way, the group never knew what line the minority participant chose.
Therefore, if the participant was going along with the group because he figured they knew the answer, under these conditions the errors should be the same as the control group that did it on their own.
HOWEVER, if conformity was due to wanting to fit in, then the level of conformity on the critical trials should be much less for the written condition, compared to the out loud condition.

Slide 8: Results: Public vs Private
So what happened when people reported on the critical trials privately? If we look at data on the % of participants who gave a wrong answer,
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it was slightly lower in the written condition, 64% compared to 76, but this is still way more than the controls. However, if we look at the % of TRIALS where participants made errors,
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it was only 12% compared to 37..
So what does this all mean?

Slide 9: Informational & Normative Influences
These results reveal that when we’re faced with group pressure, many of us will cave in. By comparing public and private responses, it appears that both normative AND informational forces were at work, although for this type of task, it was likely the normative influences that had the upper hand. Sort of like the standing ovation when you didn’t enjoy the show.
In addition to collecting data on % who conformed and % of trials where people made errors, Asch later straight up asked these guys why they went along, even though the group was making obviously wrong answers. Here’s some of what they said. *text on slide*
These statements SMACK of normative influence, motivated by fitting in with the crowd.

Slide 10: Informational & Normative Influences
So these bizarre findings from this simple experiment highlight that what the group thinks and does has a pretty big influence on how we behave.

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Tricky Topic: Altruism

Slide 1: Altruism
Altruism is a fascinating form of prosocial or HELPING behaviour, and one of the most debated. We’ll explore some of the theories and research on this fascinating topic.

Slide 2: What is Altruism?
Altruism is a SELFLESS form of helping, in which there’s no obvious benefit to the helper, and often puts them at risk
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Altruism makes no sense from an evolutionary perspective. Darwin proposed that natural selection essentially chooses traits, and their genes, which enable an individual to survive and pass on their own genes. Therefore true selflessness, especially if it comes with risk as in this helping situation shown here, is difficult to understand. Individuals who help selflessly DECREASE their own survival changes, but there are lots of examples in humans and other animals, so altruism is a puzzle from this perspective.
As you’ll learn, there are many different types of altruism. So although they’re all examples of selfless helping, they have different underlying motivations.

Slide 3: Kin Selection
Kin selection is helping our relatives. This type of helping is thought to have an evolutionary mechanism, whereby the motive is to pass on genes, even in extreme cases where the helper themselves might not survive.
We certainly see this in humans, parents will go to extraordinary lengths to help their children
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This has also been extensively studied in other species, like bee.
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Guard bees act like bouncers to regulate who gets into the busy hive, and research shows that being closely related increases the chances of getting in.
At first glance, this explanation FEELS wrong, because most people wouldn’t explain helping family members as being motivated by genetics. I mean really, are these parents helping their children because they’re thinking about their DNA?
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Are bees motivated by DNA?
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If you ask parents, they’d likely say their helping in motivated by love. Are bees motivated by love too. Who knows?
The fact that we’re able to love enough to sacrifice ourselves for our loved ones FITS with the idea of kin selection, so we end up helping our genes if though our individual reasons have nothing to do with it.

Slide 4: Reciprocal Altruism
Reciprocal altruism is a different type of helping that looks like true selfless altruism. Basically it’s tit-for-tat helping whereby we help others so that they might help us later. These monkeys will groom each other to remove bugs, and research shows that those who help most are also the greatest recipients of help from others. Reciprocal altruism can be explained in evolutionary terms because this motivation for helping promotes group connectedness and cooperation. Many social species show this type of helping behaviour.
You might have experienced reciprocal altruism yourself because advertisers and marketers KNOW that we have a strong obligation to pay help back, even if we don’t know people all that well. If you’ve felt pressured into buying something because someone has given you a sample, then that’s reciprocal altruism at work.

Slide 5: Social Exchange Theory
This begs the question, is there such a thing as true altruism?
Social exchange theory states that our helping behaviour is the product of a cost-benefit analysis. In other words, we only help when the benefits outweigh the costs. In fact, reciprocal altruism can be explained in terms of social exchange, without the need for a genetic mechanism. There are often clear benefits to helping others, feeling good about yourself or building up favours you can call on in the future.
Social-exchange theory has no problem explaining selfish helping, like when someone makes a charitable donation so that they can claim it on their tax return. What about helping someone where there doesn’t seem to be a clear benefit?

Slide 6: Empathy
One huge factor in helping behaviour is empathy, or the ability to share the feelings of others and understand their situations.
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The empathy-altruism hypothesis suggests that we help SELFLESSLY only if we can feel empathy for others.

Slide 7: Empathy and the Brain
So what does this look like in the brain? This study shown here looked at how the brain responds when someone experienced pain themselves or observed a loved one in pain. They focused on two well-established pain circuits by looking at structures involved in both the sensory AND emotional aspects of pain. The design was pretty simple, the researchers recruited couples since they reasoned that romantic partners would feel strong empathy for each other. A female participant from each couple had their brain scanned with fMRI under three different conditions, a pain-free baseline which served as a control,
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while they received a 2 sec electric shock on their right hand, or
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observed their partner get the same shock.
The researchers looked at a number of brain areas, but they focused on two key pain areas:
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the anterior cingulate cortex (or ACC), which active during emotional pain, and the somatosensory cortex (or SI), active during physical pain. The results are expressed in the graphs as a change from baseline, pain-free activity on the y-axis on the left, while time is shown along the x-axis on the bottom.
Clearly, the ACC is active during self pain shown by the green line
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AND also during observed pain of a loved one, shown in orange.
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The somatosensory cortex, on the other hand, only showed elevated activity during self pain.
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This suggests that seeing others in pain activates SOME of the same pain circuits and being in pain yourself, and the authors of this study suggested that the emotional pain circuit is used as a basis for empathy. But WHY does empathy promote altruism?

Slide 8: Why Does Empathy Promote Altruism?
Researchers suggest TWO different underlying reasons to explain the empathy-altruism hypothesis.
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The first is called egoistic motivation, whereby empathy makes us feel distressed, and helping rewards us by reducing our own distress. We know from the previous study that watching another in pain activates emotional pain circuits, which generally doesn’t feel so good.
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The other is called empathic motivation, whereby empathy promotes helpful behaviour solely to reduce the distress of another which is a reward in and of itself. This motivation is true altruism, and some researchers argue that it doesn’t exist because we relieve our own distress or guilt through helping others when we feel their pain.

Slide 9: Altruism
So, is there anything as truly selfless behaviour? Some researchers argue that most everything comes down to social exchange. This view for helping seems a bit cold and calculating, but it helps to explain how our feelings play a big role in helping behaviour.

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Tricky Topic: The Stress Response

Slide 1: The Stress Response
Stress is unavoidable, throughout our daily lives we encounter a whole range of stressful experiences, from minor hassles to major threats. This Tricky Topic will focus on how our brain and body respond to stress.

Slide 2: What is Stress?
But first, what is meant by the term STRESS? It depends on your perspective. Engineers usually think of this as physical strain on a structure or process while physiologists often define it as a state that activates the body’s “fight-or-flight” responses. Most psychologists define stress as an INTERNAL state triggered by situations that overwhelm our perceived ability to meet the demands (of that situation). Most of the time we can juggle multiple tasks just fine, but if we PERCEIVE that we have more demands that we can cope with, we can get OVERWHELMED and experience a state of stress.
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In exploring how we respond to stress, it’s first critical that we examine STRESSORS. Simply defined, a stressor is any event that triggers a stress response. Take a minute to think of some stressors that you experience day-to-day, pause this video and write them down.

Slide 3: Stressors
As you’ve likely just discovered from making your list, stress can be triggered by a variety of stressors, ranging from physically life-threatening events like your home catching on fire, to more psychologically distressing experiences like public speaking, or traffic.
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Generally, stressors fall under two classes: systemic and processive. Systemic stressors are those that pose a direct physical threat to survival, like danger from a house fire, lack of food, or severe injury. Processive stressors, on the other hand, are psychological since they don’t pose a direct threat to survival. Rather, they’re associated with threats based on prior experience and include most of the stressors we face every day lives like these stressors shown here.
The idea that there’s a connection between stress and health is certainly not a new idea, the ancient Greeks and Romans wrote extensively about the link between emotions and illness, but it wasn’t until the 1930’s that we really began to learn HOW.

Slide 4: Hans Selye
Hans Selye is credited with making the initial biological link between psychological stress and physical illness. He’s shown here in sculpture which sits on the grounds at a Hungarian-language university in Slovakia that bears his name. He was a Hungarian-Austrian-Canadian physician and scientist who started his stress research as a young professor at McGill in the 1930’s.
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He noticed that when rats are exposed to unpleasant events over a prolonged period of time, they show a wide set of symptoms, such as stomach ulcers, enlargement of the adrenal glands, and shrinking of immune tissues. What most fascinated him was that it DIDN’T SEEM TO MATTER WHAT THE STRESSOR WAS, the response was almost identical.
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For instance, in one experiment, he exposed rats to prolonged cold, by placing their cages on top of the building during winter OR prolonged heat by putting these rats in the building’s boiler room. Despite the fact these stressors put opposite demands on the rat’s bodies, they still showed these same set of responses.

Slide 5: Selye’s Main Findings
Selye made two very important contributions to the study of stress. First is that the stress response is universal in that the same set of symptoms are triggered by all sorts of stressors, like extremes in temperature, injury or scarce food resources. Also,
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this response is almost identical in humans, rats, chimpanzees, fish, and other animals. So, our response to stress is universal across various negative experiences AND across different species. Selye’s second main finding is
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that it’s chronic stress that makes us susceptible to illness. We can handle one or two stressful events relatively easily, but we start to feel the pressure when stress is repeated or prolonged and over the long term this is linked to illness.
So what happens during stress that can have such a global effect on the body? Selye’s research pointed to the adrenal glands and its hormones as the heroes AND villains of the stress response. Let’s have a look at these adrenal glands.

Slide 6: The Adrenal Gland
The adrenal glands are located just on top of each kidney. It has two main components, the adrenal cortex is the outside bit and releases a whole bunch of hormones but the one most interesting to us in the context of stress is cortisol. The inside part of the adrenal gland is called the adrenal medulla
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and it releases different types of hormones than the cortex,
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the main ones are epinephrine and norepinephrine (which are also called adrenaline and noradrenaline).

Slide 7: Physiology of the Stress Response
The physiological response to stress has two universal components that involve different parts of the adrenal gland: The HPA axis
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and the adrenal-medullary system.
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The adrenal-medullary system on the right is the connection between stress and hormone release from the adrenal medulla.
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When we’re faced with a stressor, this gets signaled to the hypothalamus which then activates sympathetic nerves. This is the body’s fight-or-flight response activated during times of threat or emergency. The adrenal medulla responds by releasing the hormones, norepinephrine and epinephrine.
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This acts to increase heart rate, breathing rate, and raises blood pressure. This fast response is thought to be important to allow quick reactions to stressors.
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On the left is the hypothalamic-pituitary adrenal, or HPA axis, which is the connection between stress and hormone release from the adrenal cortex.
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When we’re faced with a stressor, as you just learned, this activates the hypothalamus, which releases a hormone called corticotropin releasing hormone, or CRF. This travels a short distance to the pituitary gland, located just above the roof of the mouth, which releases a hormone called adrenocorticotropic hormone, or ACTH, which travels through the bloodstream to the adrenal cortex which in turn releases the hormone cortisol into the general circulation to do a number of things. It frees up energy reserves from storage, so we don’t have to pull energy out of the digestive system, which takes a long time. It also inhibits activity of the immune system. This energy liberation from reserves, and energy savings by shutting down of biologically expensive processes like wound healing, prepares the body to deal with the threat of the stressor.
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This is a slower response, not surprising since there are more steps for the HPA axis than the adrenal-medullary system.
It appears that prolonged activation of this slower HPA response is associated with susceptibility to illness. So how does this work?

Slide 8: General Adaptation Syndrome
Selye proposed the general adaptation syndrome to explain how repeated, rather than acute stress, that makes us sick. This explanation attempts to explain how the SAME stressor, which initially doesn’t cause huge health problems, leads to much larger problems later on. Selye described three stages: alarm, resistance, and exhaustion.
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In the alarm stage, the body’s resources are mobilized in response to a stressor so the SNS triggers norepinephrine release and stimulation of the HPA axis triggers cortisol release. Initially in the resistance stage, the individual copes with the prolonged stress and levels of cortisol remain high.
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Eventually, in the exhaustion stage, according to Selye, the body’s resources to deal with the stressor become depleted which results in a heightened susceptibility to illness.
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Since this was first proposed, more recent evidence pokes holes in many of the details of this model. However it remains very influential because Selye made monumental steps in understanding the link between stress and illness. Research shows that the main problem appears to be prolonged cortisol release.

Slide 9: Cortisol: The Culprit
High levels of cortisol over prolonged periods of time are associated with all sorts of problems like increased risk of depression and Type II diabetes, and suppression of the immune system. But why would our bodies respond stress to in such a way that we’d get sick? It doesn’t seem to make much sense. The best explanation comes from prominent neuroscientist and stress researcher, Robert Sapolsky.

Slide 10: Why Zebras Don’t Get Ulcers
In his book Why Zebras Don’t get Ulcers, Sapolsky describes why prolonged stress leads to illness by using an analogy that’s captured in the title. Sapolsky put it this way. Unlike humans, stress-related illnesses are actually rare in wild animals, despite the fact our stress responses are very similar. A zebra’s HPA axis isn’t all that different from ours. What IS different however, are the types of things that stress us out.
Probably the biggest stressor for prey species like the zebra is getting killed by a predator, like a lion. If a lion attacks, the zebra has to activate its stress response to give it the resources to escape. Either way, the stress response is very short-lived: it either gets caught and killed or it escapes. The zebra doesn’t activate its stress response for very long so only has a temporary spike in cortisol levels every so often. Humans on the other hand, stress about things like computers crashing or crappy wifi connections, things that are aversive but definitely not life threatening.
Why does that matter? Because these types of stressors tend to be chronic, and therefore we’re activating our stress responses all the time, and as a consequence, elevating our cortisol levels when it doesn’t really help us, like how it helps the zebra. Sapolsky says that this OVERUSE of our stress response is BIOLOGICALLY INAPPROPRIATE in our modern world, even though it was probably properly activated by our ancestors. So, in a way, a zebra is a lot smarter than a human, because it activates its stress response only in situations when it’s going to be helpful.
According to Sapolsky, what makes us sick is not our inability to deal with stressors, but rather our continued response to prolonged stress in and of itself that’s the problem.

Slide 11: The Stress Response
So the take-home message is that if you’re faced with a stressful experience take a moment to reappraise it and decide if it’s really life-threatening. If it isn’t (and it probably won’t be), try and tell yourself that it’s a waste of your resources to activate all of this biology for a situation where it’s not going to be helpful.

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Tricky Topic: Stress and the Immune Response

Slide 1: Stress and the Immune Response
This tricky topic will examine stress and the immune system.

Slide 2: Stress and the Immune System
If we look back at the physiology of the stress response we see that stress induces a long cascade of neurotransmitter and then hormonal release moving from the hypothalamus to the pituitary gland to the adrenal gland. And the adrenal gland then secretes cortisol from its cortex and epinephrine from its medulla. Once these chemicals diffuse in the body, both cortisol and norepinephrine have been shown to influence the number of immune cells produces in the body, inferring that stress can indeed affect the immune system. This is an extremely important implication for many aspects of our lives and health and sets up the point of focus for this tricky topic.

Slide 3: The Immune System
However, before moving forward we must first briefly discuss the importance of the immune system. We’ll begin by looking at 3 very basic elements involved in immune system response. The first are antigens and these are foreign substances such as chemicals, bacteria, viruses, or pollen that cause your immune system to produce antibodies against them.
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Bringing us to our 2nd important element being antibodies. And these are large proteins that bind to antigens allowing the immune system to recognize these foreign antigen substances.
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And then finally the third very basic element of the immune system would be the immune system cells themselves. And that would be killer cells primarily, of which there are 2 major types, being natural killer cells and cytotoxic T cells. And these cells bind to and destroy foreign substances mediated by this antibody binding.
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So moving on if we look at the immune system in a broader sense, it is a system of many biological structures and processes within an organism that protects it against disease, inspects the body for cells that may take on dangerous mutations, and preforms basic housekeeping functions such as cleaning up cellular debris after cellular injury. And the immune system can be subdivided into 2 basic lines of defence:
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natural immunity and acquired immunity. Now, natural immunity is the first line of defence against foreign agents, that is antigens. And it is an inborn process for removing antigens from the body. Now, this is response is usually immediate and very quick as well as non-specific, in that it will attack any antigen present. So, a quick example would be cutting your finger.
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When you cut your finger, your finger becomes very inflamed and blood vessels contract and dilate to increase the flow of blood to that area, where in addition the dilated blood vessels as well as damaged cells will release chemicals to signal for specialized immune cells to come and destroy invading microorganisms,
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thus protecting your body from the infection. So let’s say we have all our antigens entering, antibodies will then bind these and this will cue for your immune system cells
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to come and destroy these antigens from entering the bloodstream and infecting your body. The second type of immunity is acquired immunity, and this is a much more complex and it requires a number of endocrine and cellular processes. This sector will recognize specific antigens and then reproduce specialized cells or circulating proteins to fight these antigens. What makes acquired immunity unique is that it requires experience. That is, it must have had a prior exposure to a specific antigen in order to respond to it. For example, let’s say you get a cold from virus X. Your body will develop an immune response to this specific virus X such that you will be less likely to get sick when exposed to the virus X a second time.
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This might be more familiar to you when you think about the common vaccine injection in which you use to protect your body from further infection and disease. It is tapping into acquired immunity that allows this vaccine to actually work and protect your body from further infection. Moving on, what we see is that the physiological effects of stress when sustained over time will weakened both aspects of the immune system,
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where subsequently this immunosuppression will increase susceptibility to disease because of the body’s diminished ability to fight invading antigens or damaged cells. With this in mind, we will now go over some of the research that has allowed us to make these conclusions, ultimately linking both psychological and subsequently your physical health.

Slide 4: Stress and the Immune System
Research for many animal studies has shown that both psychological and physical stressors have had effects on the immune system. In particular, stressors on animals, including
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mental stressors, maternal stressors, inescapable shock, abrupt temperature change, loud noise, and many more. Following this, what all these studies have shown
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is that they’ve seen a reduction in responses to antigens, a reduction in the number of immune cells present, and an overall decrease of immune system function.
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Following this, some studies have looked at naturally occurring stressors in human subjects and correlated changes in these individuals’ respective immune system functioning. Natural occurring stressors
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such as final exams, sleep deprivation, loud noise, divorce, and caring for an Alzheimer’s or AIDS patient have all been studied and shown collectively, again, to produce
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reductions in immune system response or function.
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Following these results, it is important to note that these studies infer that stress can indeed cause reduction in immune system functioning, but it has not told us whether or not this necessarily effects the actual health of the individual. This last question is asked and answered in the following 2 experiments we’re going to look at.
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In the first experiment, formed in 1995, two different groups were assembled. The first group, group A, was of individuals who were currently the primary care providers for individuals with Alzheimer’s disease and the second group, group B, was a control group. So this presumed that those taking care of individuals with Alzheimer’s disease would have higher levels of psychological stress. Following this,
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each individual within each group was given a small puncture wound and followed up by assessing 2 separate factors.
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The first was testing for the concentration for different immune variables in the blood, that’s measuring the immune system response. And the second looked at the actual wound healing process, so the amount of time it actually took for the small puncture wound to heal, thus measuring the actual direct health of the individuals.
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In both cases what they found, first pertaining to the immune variables in the blood, was that group A patients had significantly fewer than group B. As well with wound healing, it actually took much longer for group A to have these small wounds heal than those in group B. This suggests that stress does induce diminished effects in the immune system, subsequently resulting, as shown here, directly effecting the health of the individual as well. Where here it is exemplified by actual healing of the small puncture wound.
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Following this in the second study, researchers took a group of individuals and assessed them on 3 aspects of their lives. These were their self-reported amount of perceived stress that they experienced, the amount of external stressors as determined by the researchers, and then finally the social networks they had available to them. They then exposed individuals to the common cold
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and determined their susceptibility to it. In conclusion, they determined that the most prominent predictor of whether or not an individual got sick was their perceived level of stress.
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This tells us that it is the individual’s own subjective experience of the level of stress they’re experiencing that determines its effect on the immune system and thus their health.

Slide 5: Stress and the Immune Response
That concludes this tricky topic looking at stress and the immune system. Thank you for listening.

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Tricky Topic: Diagnosing Psychological Disorders

Slide 1: Diagnosis
Diagnosing psychological disorders is a tricky topic indeed, but before we dive into the issues surrounding diagnosis, it’s important to first consider a more basic question: How can we distinguish different behaviour from disordered behaviour.
Let’s consider some historical examples of extreme behaviour, and evaluate these cases as different or disordered.

Slide 2: Different or Disordered
Take post-impressionistic Dutch painter Vincent Van Gogh, he’s one of the best known and most prolific artists of his time. He created over 2000 works of art, in a career that lasted only ten years. This painting entitled” Self-Portrait with Bandaged Ear and Pipe” is a glimpse into his unusual behaviour. Van Gogh did this painting after having an argument with a friend, and, in a fit of rage, took a razor and cut off the lower portion of his left ear. He then wrapped the earlobe in a newspaper and gave it to a prostitute named Rachel, telling her to “keep this object carefully”
So for a bunch of reasons, van Gogh was certainly different than most other people: on the one hand he produced some of the most influential works of art. But in his personal life he was prone to extreme and unstable behaviour. The painting above is one demonstration of his self-harming behaviour, and he eventually died by suicide.
There is much speculation about the cause of Van Gogh’s unusual behaviour, he had several major depressive periods as well as manic and psychotic episodes, so most people agree that he likely suffered from mental illness.
Let’s consider another case.
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Witold Pilecki (VEE-Told PILET-SKI) was a Polish soldier and founder of the resistance movement in German-occupied Poland. He was VOLUNTARILY imprisoned at Auschwitz in order to secretly report on what was happening there. He stayed for 2.5 years and later escaped. This behaviour is certainly different than what most people would do. This mugshot here however is NOT from his time at Auschwitz, but when he returned back to Poland, and was accused of treason.
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He was imprisoned, tortured, and executed, not by the Nazis, but by the Soviet-backed Polish government. This photo was taken at his trial, and although he doesn’t look happy, he also doesn’t look disheartened.
Like Van Gogh, Pilecki’s behaviour intentionally caused him harm, no doubt about it. But the circumstances and motivation for his actions means that history remembers him as heroic, not disordered.
These two examples highlight the challenge in distinguishing different (in the case of Pilecki) from disordered (in the case of Van Gogh).

Slide 3: The Medical Model
The current theory and practice of diagnosing mental illness has been heavily influenced by the MEDICAL model, which states that mental illness is best diagnosed and treated as a MEDICAL illness
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This perspective on mental illness contrasts earlier views that considered mental illness to be caused by moral weakness or even demon possession and treatments often involved extreme measures like drilling holes in the head to release evil spirits, like in this 5000-year old skull
The MEDICAL MODEL is certainly a move in the right direction based on the evidence we have about the biological basis of psychological disorders, but the medical model presents some of its own challenges.

Slide 4: Difficulty in Diagnosis
Let’s take an example of a clear, physical medical problem, a deep cut in the finger. A physician can tell, without even talking to the patient, what’s wrong and how to treat it – clean the wound to prevent infection, stitch it up, and bandage it. Easy. But some physical conditions aren’t so obvious just by looking at someone.
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Take a heart arrythmia, or irregular heart beat. You can’t tell just by looking at someone whether they have a heart arrythmia,. A doctor can talk to the patient, and get some idea about symptoms. But it’s not as obvious what’s wrong, like with a finger wound. Using a simple device, like a stethoscope, or an ear to the chest, lets the physician know what’s going on.
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What about someone suffering depression? Certainly you can tell by looking at this man that there’s something wrong, but maybe his hockey team just lost the final. Maybe he’ll get over it. Maybe he’s been feeling this way every day for months.
Clearly, It’s necessary to TALK to the person for some time to differentiate DIFFERENT from DISORDERED so diagnosing psychological disorders involves a bit of a judgment call. We can’t tell just by looking at someone what’s going on, and we don’t have any devices to tell us definitively what’s wrong.
So what information do diagnosticians like psychiatrists and psychologists use to make their decisions?

Slide 5: History of Diagnosis
One of the first attempts to provide some guidelines about diagnosis was by German psychiatrist Emil Kraepelin. In his publication, Compendium der Psychiatrie in 1883, he put disorders into categories so that diagnosis could be standardized and measured. It wasn’t until 1952 that a similar attempt was made in North America by the American Psychiatric Association (or APA) with the Diagnostic and Statistical Manual of Mental Disorders. The DSM has become the standard in NA for psychiatrists, psychologists, medical insurance companies, and others involved with diagnosis. Let’s look at the history.

Slide 6: A Work in Progress
The DSM can be, and should be, considered a work in progress. The 1952 edition was the 1st NA classification, and was about 130 pages in length.
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The DSM II was published in 1968, with some modifications to the original, but not a lot added to the length of the document.
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The DSM III came out in 1980, with a revision, the DSM III R, in 1987. This was revamped to make the guidelines consistent with other tools, like the International Classification of Diseases, or ICD, used by the WHO. This update greatly increased the size of the document and the number of disorders.
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The DSM IV came out it 1994, followed by its revision the DSM IV TR (for text revision) in 2000. This attempted to provide clearer diagnostic criteria and emphasized an empirical, evidence-based approach. This greatly increased the length of to 886 pages.
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Most recently the DSM 5, which ditched the Roman numerals, came out in 2013 and there were some changes to how disordered behaviour is viewed. In previous versions there were separate axes to consider, but this was replaced by a dimensional approach that places behaviours, thoughts, and emotions along a continuum. This most recent revamp also increased the length, so the current version is 947 pages in length.
Although the DSM is a useful tool for treatment providers, it is not without criticism.

Slide 7: Criticisms of the DSM
One criticism is that the DSM medicalizes normal human behaviour, by labelling normal reactions to life events, such as sadness after losing a loved one, as mental illness. (CLICK) The DSM 5 did make an attempt to address this to some extent by introducing a dimensional approach, so diagnosis considers the grey area and is not based strictly on ”yes” or “no” categories. However the dimensional tools have only been developed for some but not all disorders.
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Another criticism of relying on the DSM for diagnosis is that it has a strong North American perspective, and some argue that the American Psychiatric Association (APA) has had too much influence. Another classification system developed by the World Health Organization is the International Classification of Diseases or ICD. This is used for diagnosis of all sorts of disorders, not just mental illness, and has also gone through many revisions. The ICD-11 was developed in 2018 and takes effect in 2022.
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Lastly, some take issue with the idea of mental illness altogether because it ignores moral and social norms, which have a big influence on whether behaviour is considered abnormal or not. Thomas Szasz was an American psychiatrist and academic who challenged the very idea of mental illness in his books The Myth of Mental Illness and The Manufacture of Madness. He argued that mental illnesses should be considered problems of living rather than defined diseases. For instance, poverty is associated with substance abuse, but the DSM considers addictive disorders as a problem with the individual, not society.

Slide 8: Stigma of Mental Illness
Another problem in diagnosing mental illness is the stigma surrounding it, because as a society we have a tendency to judge people with psychological problems and this can lead to negative stereotypes.
This is an enormous barrier since it means that people often don’t want to admit they’re suffering from mental illness and might be hesitant to seek professional help. It also means that people might not get social support they need from their friends and family, which is really, really important in overcoming psychological disorders.
A number of initiatives, like Bell’s Let’s Talk Mental Illness, have tried to raise awareness and reduce stigma and has been championed by Canadian Olympian Clara Hughes. She won medals in both cycling and speed skating but suffered from bouts of depression and struggled with alcoholism throughout her life. By talking openly about her own struggles, and how sports helped her overcome them, she is trying to change the way that society views mental illness.

Slide 9: Diagnosis
So this summarizes both the history of diagnosing psychological disorders, and some of the challenges faced in trying to make a meaningful diagnosis.

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Tricky Topic: Diathesis-Stress

Slide 1: Diathesis-Stress
The diathesis-stress model of mental illness is an old idea described by many different names. Essentially it tries to address the age-old debate of what causes illness, is it nature or nurture? Or can we find the best explanation if we consider both?
There are a number of explanations for causes of psychological disorders, and one disorder that has received a lot of attention is depression. After so many years of research, we’re starting to get some hints that depression has multiple causes.

Slide 2: Diathesis + Stress
We know that family history is a risk factor for depression, NO DOUBT ABOUT IT, and certain genes have been identified as culprits, so biological make-up appears to be important. Also, there have also been a whole slew of life events associated with episodes of depression, and what these events all share in common is that they’re stressors.
Diathesis is the Greek word for “predisposition” and the diathesis-stress model includes both biological AND environmental influences on developing a psychological disorder. It suggests that biology, or NATURE, and psychology, or NURTURE INTERACT to influence the occurrence of mental illness.

Slide 3: Research Question
One study that directly tested the diathesis-stress model attempted to answer the following question:
Why do stressful experiences trigger depression in some people but not others?
These researchers conducted a large scale, longitudinal study to look at the influences of genes and life events. They focused on the serotonergic system since it’s been implicated in depression.
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This is a schematic of a typical synapse, where neurotransmitter is released and binds to receptors on the postsynaptic side.
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This here is the serotonin transporter, which is the recycling protein that takes serotonin out of the synapse and repackages it into vesicles. IT turns out that the gene that makes this transporter protein comes in two forms,
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short and long, which work with slightly different efficiencies. We get one copy of this gene from each of our parents, which means there are three possible combinations of these genes,
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short-short, short-long, and long-long.
So how does this little tiny protein made by different forms of a gene tell us anything about stress and depression? Let’s have a look at the study design.

Slide 4: Study Design
This diathesis-stress study was part of a much larger Dunedin Multidisciplinary Health and Development Study, conducted in New Zealand. This study is unique because it uses a longitudinal design – following participants for decades and has at least an 80% participation rate, which is unheard of with this large a sample over this long a time period. However, the researchers were able to get the participants engaged and on board, so they’ve been able to ask lots of interesting questions as new information has become available.
In this particular study, participants were 1037 people from a 1972 birth cohort, 847 of which were followed up every two years when they were kids, and then every 3-5 years from adolescence. For this study the researchers focused on these people when they were young adults. They took DNA samples at age 26,
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so they could find out which serotonin transporter genes they had, and also measured depression symptoms through a clinical interview.
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They compared this to life events that happened between the ages of 21-26, which was collected using a life history calendar. And they found something very interesting.

Slide 5: Findings
In this figure, the number of stressful life events is shown on the x-axis on the bottom, and the likelihood of a depressive episode is represented on the y-axis on the left.
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For those in the cohort with low levels of life stress, there was a very low incidence of depression, regardless of the types of serotonin transporter genes. HOWEVER, this was very different for people who reported higher levels of stress, when genes REALLY seem to matter. With 4 or more stressful life events, those with two copies of the short gene were most likely to get depression
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followed by those that had one short and one long, and finally those that had two long copies of the gene.

Slide 6: Support for Diathesis-Stress
There is mounting support for this nature plus nurture explanation for many disorders, in addition to depression, like Alzheimer’s disease, schizophrenia, and ADHD. Some scientists now think diathesis-stress might explain the large individual vulnerability in mental illness.

Slide 7: Diathesis-Stress
Using a unique sample of participants followed over time allowed researchers to test the idea of stress-diathesis in the development of depression, but this is becoming accepted as a model to consider in the development of other psychological and physical disorders.

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Tricky Topic: Causes of Schizophrenia

Slide 1: Causes of Schizophrenia
Schizophrenia is one of the most debilitating psychological disorders so there’s a lot of interest in trying to identify potential causes. It’s categorized as a psychotic disorder, so we’ll describe some of the general characteristics of these types of disorders and their symptoms before focusing on causation.

Slide 2: Psychotic Disorders
Psychotic disorders are disorders of thought and perception and in particular an inability to distinguish between what’s real and what’s imagined. Sometimes we all think things happened in a way they didn’t, or hear or see things that aren’t actually there. For most of us. These unusual situations are normal but rare. In people with psychotic disorders these false beliefs and disconnection from reality become pervasive and debilitating.
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Schizophrenia is the best known and the most prevalent of the psychotic disorders and means SPLIT MIND, meaning the mind is split from reality. This is best illustrated by reviewing the symptoms of this disorder.

Slide 3: Symptoms of Schizophrenia
The DSM 5 diagnostic criteria for schizophrenia include five symptoms.
Delusions are thoughts and beliefs that aren’t consistent with reality. Probably the most problematic are paranoid delusions, where the schizophrenic person believes that others mean to cause harm. However, delusions can also involve exaggerated claims of power or knowledge, such as claims of mind reading ability or communication with higher powers. These are called delusions of grandeur.
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Hallucinations involve false sensory perceptions, most often auditory in the form of hearing voices, but they can also be visual or tactile sensations. These first two symptoms often prompt people to seek treatment.
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Another symptom is disorganized speech, such as tangential speech where the speaker loses focus and wanders without returning to the original topic. Disorganized speech can also take the form of “word salads” where the speaker follows grammatical rules but makes little sense. According to the DSM, a confirmed diagnosis of schizophrenia must include one of these first three symptoms.
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Disorganized or in some cases, catatonic behaviour, where the person remains unresponsive and immobile for long periods of time, is another symptom of schizophrenia.
Because these symptoms involve the PRESENCE of thoughts and behaviours characteristic of schizophrenia, and are NOT commonly seen in people without the disorder,
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they are referred to as POSITIVE SYMPTOMS. The fifth category in the DSM diagnostic criteria is NEGATIVE symptoms
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which refers to the ABSENCE of behaviours displayed by non-schizophrenics, such as reduced emotional expression, social withdrawal, low motivation, and lack of pleasure. These negative symptoms are present in 20-40% of people with schizophrenia, and tend to be difficult to treat.
Although not officially included in the DSM diagnostic criteria, about 80% of schizophrenics experience cognitive symptoms or problems with information processing. This includes
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impairments in verbal memory, working memory, processing speed, and attention. Although these symptoms are common, they’re difficult to confirm in a diagnostic interview, since catching them requires intensive cognitive testing, which requires special training to administer and can take hours to complete.
These three sets of symptoms are widespread, so it’s a good bet that this disorder affects the functioning of the brain in a big way, so not surprisingly, there are multiple proposed causes. Most explanations of the causes of schizophrenia combine nature and nurture.

Slide 4: Nature and Nurture Explanations of Schizophrenia
There’s a strong heritable component to schizophrenia, since there’s increased risk if first degree relatives have the disorder. There have been over 19 potential genes identified, but that’s not to say that certain genes CAUSE the disorder.
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Different disruptive early life events have also been implicated as a cause for schizophrenia, especially if they happen at critically important developmental periods since the young brain appears to be vulnerable. So having a combination of family history with certain negative early life events greatly increases risk for the disorder. So what specifically are some of these early life events?

Slide 5: Early Life Events
There is a well-demonstrated link between many types of early life abuse or neglect and psychotic symptoms. A child who experiences physical, emotional, or sexual abuse is more likely to develop schizophrenia than children who don’t, particularly if they have a parent with the disorder. Events that happen before birth are also associated with increased risk, so maternal health during pregnancy has also been the focus of research
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Certain infections such as toxoplasmosis, rubella, herpes are associated with increased risk as well as pre-natal depression. Heavy use of psychoactive drugs, particularly in adolescence also raises concern
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since there is a well-established association between early marijuana use and later psychosis. Marijuana use in early adolescence increases the risk of later developing schizophrenia or other psychotic disorder roughly 5-10 times, although this does not seem to be the case for people who start using marijuana late in life. This research is important with the plans for legalization of recreational use in Canada, and has led to much discussion around what the legal age should be.
It’s important to note that these risk factors are just that, they increase RISK. Many people experience adverse events in childhood, their mothers contract infections while pregnant, and they used marijuana as young adolescents, but never go on to develop schizophrenia. However, each of these risk factors, paired with a family history of the disorder makes it more likely to occur.
Clearly schizophrenia itself is complex, and the potential causes are many and often debated. What is agreed upon however, is that this disorder affects brain functioning. We’ll consider some of the neuroanatomical and neurochemical abnormalities observed with the disorder.

Slide 6: Schizophrenia & the Brain
Schizophrenia is associated with an overall reduction in brain volume compared to people without the disorder. Although there is some debate about the exact nature of these brain differences and whether they’re a cause or consequence of the disease, several areas have been consistently found to be smaller: the prefrontal cortex in the frontal lobes, the superior part of the temporal lobe, and several limbic areas not visible in this image, the anterior cingulate cortex, the hippocampus, and the amygdala.
One of the most striking consequences of this loss of brain tissue in schizophrenics is enlarged ventricles, a hallmark feature of schizophrenia.

Slide 7: Enlarged Ventricles
Ventricles are the spaces in the brain that produce cerebral spinal fluid. These images are brain scans of two identical twin brothers; the unaffected brother on the left did not show symptoms of schizophrenia, while the affected brother on the right did. The arrows are pointing to the butterfly-shaped VENTRICLES, which are clearly much larger in the affected twin. Keep in mind that larger ventricles means less surrounding brain.
The loss of brain tissue in schizophrenia shows up quite early, and there’s evidence that it might precede the appearance of symptoms, so some believe that this neuroanatomical change might be an important causal factor of the disease. In addition to these potential neuroantomical causes, there are also well-accepted neurochemical changes in schizophrenia that contribute to symptoms. There are two major neurotransmitter systems implicated in symptoms of schizophrenia.

Slide 8: Neurochemistry of Schizophrenia
The dopamine hypothesis is based on two pieces of evidence. First, drugs that trigger large amounts of dopamine release in the brain, like amphetamines, actually trigger symptoms similar to schizophrenia, particularly hallucinations and delusions. Second, dopamine antagonists, drugs that block dopamine receptors, are effective in treating many symptoms of the disorder, like hallucinations and delusions. There are some problems with the dopamine hypothesis however, in that it seems to play a role in positive symptoms, but does not seem to explain the other symptoms.
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More recent research has suggested that glutamate deficiencies contribute to schizophrenia since drugs that block the NMDA glutamate receptor, like PCP (also known as angel dust) and ketamine (also known as vitamin K) cause hallucinations ad other symptoms, so it shouldn’t be surprising that glutamate might play a causal role. The glutamate story is somewhat complicated since the effects of low NMDA activity in some parts of the brain appears to result in ENHANCED amounts glutamate in other areas. Therefore drugs that reduce the glutamate activity at non-NMDA receptors have been considered as possible treatments, although none of these are currently used as standard treatment. Glutamate seems to be involved in ALL of the different types of symptoms of schizophrenia,
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positive, negative, and cognitive and so glutamate drugs, possibly co-administered with dopamine antagonists, might prove to be useful in the future. A note of caution however, that glutamate is the most abundant excitatory neurotransmitter in the brain, involved in widespread functions, so altering its activity in the human brain to treat ONLY schizophrenic symptoms is not straightforward.

Slide 9: Causes of Schizophrenia
So although there’s no clear answer about what causes schizophrenia, there are a number of hints that genetics, early life environment, neuroanatomy, as well as neurochemistry are all possible contributors. This information has directed how we think about schizophrenia and have guided treatment approaches.

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Tricky Topic: Mood vs. Personality Disorders

Slide 1: Mood vs. Personality Disorders
Today, we’re going to look at psychological disorders. We’re going to focus on personality disorders and mood disorders. We’ll look at how they’re different and what each entail.

Slide 2: Personality vs. Mood Disorders
First, we have to understand the fundamental differences between personality disorders and mood disorders. A personality disorder is a maladaptive and inflexible pattern of cognition, emotion, and behaviour, within an individual. Another way to put this is that personality disorders are fundamental differences in how a person experiences or deals with emotions, how they interact with others, and how they think about problems or interpret situations. It’s important to note that personality disorders generally develop in late childhood and adolescence and continue into adulthood, as they are often permanent in nature. In contrast to personality disorders, mood disorders are a category of psychological disorders characterized by severe disturbances in emotional behaviour. And remember that in order for someone to be diagnosed with a disorder, their feelings or patterns of behaviour must either be causing significant distress in the affected individual or be significantly negatively affecting their day-to-day functioning.

Slide 3: Personality Disorders
First, we will look at personality disorders, of which there are 3 distinct clusters.

Slide 4: Odd-eccentric
The first cluster is odd/eccentric, of which there are 3 subtypes. The first is schizoid personality disorder, and this is someone who does not want close relationships, is emotionally aloof, reclusive, and often humourless. This is an individual who really wants to live a solitary life. The second subtype is schizotypal, which is someone who is really isolated and asocial, someone who has odd thoughts and beliefs. For example, this individual might look at stories on tv and in the news and believe that these stories are about them, even though they have no relation at all to the stories being shown. The third subtype is paranoid personality disorder, and this is someone who is extremely suspicious and mistrustful of people in both ways that are unwarranted and not adaptive. An example here would be someone who holds unwarranted grudges for an unusually long period of time.

Slide 5: Dramatic-emotional
The second cluster of personality disorders are dramatic emotional, of which there are 4 subtypes. The first is histrionic personality disorder. This is someone who wants to be the centre of attention at all times, and will achieve this either through dramatic, seductive, flamboyant, or extremely exaggerated behaviours directed towards others. The second subtype is borderline personality disorder. This is an individual with out of control emotions, as well as having a fear of being abandoned by others. By doing this, these people will often oscillate between idolizing and despising people who they are close with. The third subtype is narcissistic personality disorder. This describes an individual who has extremely positive self-image, is extremely arrogant, and has exaggerated self-centred thoughts and ideas. The fourth type is antisocial personality disorder, and this is someone who is extremely impulsive, deceptive, often violent and ruthless, and callous in their behaviour. This is a very serious and potentially dangerous disorder. However, it’s really important not to confuse antisocial personality disorder with someone who is asocial, where being asocial just means someone who is shy and does not necessarily enjoy themselves in social situations.

Slide 6: Anxious-fearful
The third and final cluster of personality disorders is anxious/fearful, of which there are 3 subtypes. However, in general, this third cluster is described by someone who has a persistent high level of anxiety and nervousness as well as fear in many different situations and contexts. The first subtype is avoidant personality disorders, and this is someone who is so afraid of being criticized that they will avoid interacting with others and become completely socially isolated. The second is dependent personality disorder. This is someone who has a great fear of being rejected, resulting in the development of extremely clingy and dependent relationships with others such that they only feel safe when in these relationships with others. The third is obsessive compulsive personality disorder, which is someone who is very rigid in their habits and tend to be extreme perfectionists. This is similar to but much more general than OCD, or obsessive-compulsive disorder. Here we are looking at obsessive compulsive personality disorder, which is different than obsessive compulsive disorder, where obsessive compulsive disorder is a CLINICAL disorder, and is much more specific to certain actions, such as cleaning, or tapping a certain amount of times. On the other hand, obsessive compulsive personality disorder is much more general to all aspects of one’s lives.

Slide 7: Depression
Now we’ll look at mood disorders. Mood disorders are a category of psychological disorders characterized by a severe disturbance in one’s emotional behaviour. These disturbances in emotional behaviour are so severe that they prevent people from functioning normally. We’re going to look at 2 common mood disorders, those being depression and bipolar disorder. First, looking at depression, it’s important to note that it manifests differently in different people. However, in general, it can be categorized as any combination of intense sadness and anxiety and extreme apathy and discontent. So, the first type that we’re going to look at is major depressive disorder. This is a mood disorder characterized by pervasive low mood, lack of motivation, low energy, and feelings of worthlessness and guilt that lasts for at least 2 consecutive weeks. This is also often associated with sleep disturbances, such that people will suffer either from insomnia or hypersomnia, which is an excess of sleep. More than often, it reoccurs in someone’s life. It’s very important to highlight that this is more than just the blues. When we look at major depressive disorder, we’re talking about a life-altering changes in one’s behaviour, accompanied by a deep apathy and withdrawal from one’s life. This can be a major risk factor for suicide. Dysthymia, on the other hand, is a form of depression that is milder in intensity than major depressive disorder. The symptoms are the same as the former, however, they are less intense. Clinical depression occurs in about 12% of Canadian adults at some point in their lives, so it is quite pervasive.

Slide 8: Causes of Depression
When looking at the causes of depression, it’s important to understand that there are both external and internal factors that increase the likelihood of experiencing a depressive episode and there was a study done in 2003 by Caspi and colleagues that illustrated these points. To briefly explain this experiment, they measured both the number of stressful life events that participants experienced, representing extrinsic factors, and a person’s genetic propensity for depression, representing intrinsic factors. This experiment showed that it was an interaction between BOTH extrinsic stressful life events AND intrinsic genetics that determines one’s probability of experiencing depression.

Slide 9: Bipolar Disorder
The second type of mood disorder that we’ll discuss is bipolar disorder. This is characterized by extreme periods of depression that alternate with episodes of highly elevated mood and intense activity, referred to as mania. During manic episodes, people will typically experience a huge spike in energy, sleeplessness, delusions of grandeur, racing thoughts, and impulsivity. However, a common misconception about bipolar disorder is that individuals with bipolar disorder frequently alternate between high and low mood, even multiple times per day or hour. The reality is that the depressive phases and manic phases last for extended periods of time. A patient may experience depression for months and then mania for a month.

Slide 10: Causes of Bipolar Disorder
Just like depression, there are both external and internal factors that increase the likelihood of experiencing bipolar disorder. External factors include the external environment during development, starting as early as the fetal stage. For example, fetuses exposed to large amounts of alcohol are put at increased risk for developing bipolar disorder later in life. In terms of internal factors, many have been identified, including a genetic component to bipolar disorder. In twin studies, results have shown that if one twin has bipolar disorder, there is a 40-70% chance that the other will also at some point in their life experience bipolar disorder.

Slide 11: Mood vs. Personality Disorders
That concludes tricky topic, covering different types of mood and personality disorders and how they differ from one another.

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Tricky Topic: Psychological Treatments

Slide 1: Psychological Treatments
Welcome to the Tricky Topic on psychological treatments. In this tricky topic we will take specifically about a number of different types of treatments for psychological disorders that fall under the category of psychological-type treatments.

Slide 2: Treatment of Psychological Disorders
Treatments for psychological disorders can be broken down into 3 broad categories. These are psychological treatments, including various approaches like psychodynamic, humanistic, behavioural, cognitive-behavioural, and group, which we will discuss today. The second category of treatment for psychological disorders is biological treatments, which includes things like drug therapy, psychosurgery, and electric and magnetic therapies. And finally, we can combine these two approaches for things like integrative therapies, and mindfulness and psychotherapy to try and maximize the efficacy of biological and psychological treatments so that an individual can have the best chances of recovery.
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For this tricky topic, however, we will be focusing on the psychological treatments.

Slide 3: Psychodynamic Theory
Let’s first take a look at the psychodynamic approach. The psychodynamic approach was first developed by one of the most famous early psychologists – Sigmund Freud. Since its inception, psychodynamic theory has undergone a number of changes, but at its core it still focuses on tapping into a person’s unconscious thoughts and feelings and interpreting their meaning with the help of the therapist.
One of the most common techniques employed by therapists using the psychodynamic approach is something called “free association”. Free association simply involves having the individual just start talking about whatever comes to their mind – they don’t need to understand it or interpret it, they just need to talk. Some therapists will then try to “interpret” the underlying meaning behind these statements, while others use this technique simply to relax the client and help them to become more comfortable with the situation.

Slide 4: Humanistic Theory
Humanistic theory is based around the central ideas of empathy and helping an individual reach their greatest potential. The purpose of the therapist is to listen, empathetically, and ensure that the client feels listened to and not judged in any way. The hope is that through this unconditional positive regard from the therapist, the client will start to see themselves as having more self-worth and potential to achieve their goals.

Slide 5: Behavioural Therapy
Behavioural therapy is very different from both psychodynamic and humanistic approaches in that the primary focus is on changing the behaviour rather than the thoughts and feelings. Behavioural therapists use a number of different techniques to change behaviour, relying on the principles of operant and classical conditioning approaches.
Some examples include token economies (essentially reinforcing good behaviour with a token that can then be exchanged for some kind of privilege) – often used with children.
And systematic desensitization – a process that is often used to treat issues like phobias. Desensitization involves exposing an individual to increasing more intense versions of the thing they fear, allowing the person to experience the fear but face the item long enough that they can then return to a state of relaxation. Once a person becomes comfortable with the stimulus, the therapist increases the intensity and repeats the process.

Slide 6: Cognitive and Cognitive Behavioural Therapy
Cognitive and cognitive behavioural therapies are very popular forms of treatment for psychological disorders. And, as we’ll see in a moment, are considered some of the most effective treatments available for many types of disorders.
Cognitive therapy involves the therapist working with the client to identify the maladaptive thoughts and then challenges them – helping them to eventually fix these erroneous thoughts.
Cognitive-behavioural therapy is just like it sounds – it incorporates the techniques from both cognitive therapy and behavioural therapy to modify a person’s maladaptive thoughts and behaviours. For example, it might involve having a person identify their erroneous thoughts, but then going the extra step of introducing a reward (a technique from the behavioural camp) to reinforce the modified behaviour.

Slide 7: Group Therapy
Finally, group therapy involves a group of individuals with a similar challenge or issue, coming together and meeting as a group with a therapist. Through discussion, individuals in the group get to share their experiences, hear others experiences (helping them to realize they’re not alone) and learn how each individual is coping with their challenges or working through them.
Group therapy can be an excellent source of support and allow a venue to air frustrations or work through problems with others.

Slide 8: Efficacy of Treatments
So, how well do these treatments actually work?
This graph, originally created by Epp and Dobson in 2010 and later reproduced by Beck and Dozois in 2011, outlines the efficacy of CBT and exposure therapies in treating a number of different psychological disorders. We can see here if we look at the absolute efficacy of some of these different types of treatments, Two pluses means it is the number one best treatment for that disorder and one plus means there is evidence that this treatment has positive effects. So we can see, for example, that for specific phobias, exposure therapy is the best possible approach that we can be using for this specific disorder. Same with panic disorders, exposure therapy works very well. And then you can see a number of disorders where cognitive behaviour therapy is really quite an effective treatment, for things like depression, bulimia, eating disorders, schizophrenia.
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And we also look at the efficacy relative to some of the biological approaches like medication, in many cases cognitive behavioural therapy is just as good if not better than medications. So we know that CBT is incredibly effective for many types of disorders and often times is used in addition to or paired with a biological treatment to try and get the most out of that treatment and to try and help and individual as much as possible.

Slide 9: Psychological Treatments
In this tricky topic, we’ve briefly covered some of the approaches to psychological treatment of disorders. Thank you for listening.

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Tricky Topic: Biological Treatments

Slide 1: Biological Treatments
Today we’re going to look at the biological treatment of depression, specifically using drugs to treat depression. A number of psychological disorders have been shown to correlate with brain changes and specific neurotransmitter signalling pathways. Therefore, many treatments focus on drug therapies aiming to restore neurotransmitter signalling back to biologically normal levels. It’s important to note that the drugs used to treat psychological disorders are the second most prescribed drug class in Canada, where the largest drug class prescribed is for cardiovascular disease.

Slide 2: Depression and Monoamine Neurotransmitters
Depression has been shown to correlate with a decrease in serotonin as well as other monoamine neurotransmitters in the brain.
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As just explained, many therapeutic approaches have used drug therapy to try and restore monoamine neurotransmitter levels within the synaptic cleft to a functional level.
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There are 4 main monoamine neurotransmitters that have major roles throughout the brain. Decreased levels of these monoamines have been shown to correlate with depression. These are serotonin, dopamine, norepinephrine, and epinephrine. They’re classified by the fact that they share common synthesis pathways and all possess a common amino functional group in their chemical structure- each is an amine containing only one amino group.
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As previously mentioned, each of these specific neurotransmitters have very wide-spread distributions throughout the brain.
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When we first look at serotonin, we see a wide distribution throughout the midbrain, frontal cortex, and throughout the entire cortex as well as the cerebellum.
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Following that, if we look at dopamine, it has a lot of diffusion throughout the midbrain as well as the frontal cortex.
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Norepinephrine again like serotonin is found throughout the entire brain in all major structures.
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And then finally epinephrine is mostly concentrated in the brain stem.
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A decrease in monoamine neurotransmitter release in the brain is believed to be the main molecular mechanism by which depression manifests in the brain. Currently there are 3 main antidepressant drug classes that work to increase monoamine transmitter levels in the brain. Those 3 classes are monoamine oxidase inhibitors, tricyclic antidepressants, and selective serotonin reuptake inhibitors.
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Each class differs from one another in 2 main ways. The first being its specificity and the second being its mechanism of action. The next question following this would be how do these specific drug classes increase monoamine neurotransmitter levels in the brain? Before looking at how these specific antidepressant drugs work, we first need to review the basic mechanisms guiding synaptic transmission, reception, and degradation of monoamine neurotransmitters.

Slide 3: Synapse
If we look at our synapse, what we see is, in the order of events of synaptic release, we first have our monoamine neurotransmitter that is loaded into presynaptic vesicles in the terminal of the presynaptic axon. These synaptic vesicles are then taken to the membrane where they fuse, resulting in the release of these neurotransmitters into the synaptic cleft. At this point, these monoamine neurotransmitters will bind to postsynaptic receptors, causing a response in the postsynaptic cell. Following this, these receptors will either become saturated, or they release this monoamine neurotransmitter back into the synaptic cleft, where it will then be reuptaken by reuptake transporters.

Slide 4: Monoamine oxidase Inhibitors
Once back inside the presynaptic cell, these monoamine neurotransmitters will then be degraded by monoamine oxidase. Monoamine oxidase is an enzyme that breaks down any monoamine neurotransmitters so that it can be resynthesized as the cell needs it and then the cycle continues.
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If we look at our first drug class, that’s the monoamine oxidase inhibitors, which reduce the actions of the enzyme monoamine oxidase. As just discussed, this is a major enzyme in the breakdown of monoamine neurotransmitters. By blocking monoamine oxidase, there will be an increase in monoamine neurotransmitters available,
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ultimately leading to increased release in the synaptic cleft
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and subsequent receptor binding and therefore a greater response than normally elicited by the lower levels of these monoamine neurotransmitters when monoamine oxidase is allowed to be active.

Slide 5: Tricyclic Antidepressants
The second class is tricyclic antidepressants. These specifically block presynaptic reuptake of serotonin and norepinephrine in particular. When this happens, this causes, again,
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a build-up of these monoamine neurotransmitters, specifically serotonin and norepinephrine in the synaptic cleft
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and subsequently increased binding to the postsynaptic receptors.

Slide 6: Selective Serotonin Reuptake Inhibitors (SSRIs)
Finally, the third class is selective serotonin reuptake inhibitors. These are really interesting because there is a lot of evidence put forth that suggested that the monoamine neurotransmitter serotonin is especially and more significantly than the others involved in depression. This drug was developed that selectively targets serotonin, resulting in the selective increase of serotonin in the synaptic cleft. The aim was to result in a drug that still produced beneficial results for the treatment of depression while reducing side effects. Due to the blockage reuptake pumps that transport serotonin
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we have an increase of serotonin in the synaptic cleft,
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and then an increase in the binding to these postsynaptic receptors, trying to bring them back to the normal endogenous levels or the normal endogenous effect of serotonin that would be present in the brain of an individual that is not suffering from depression.

Slide 7: Depression and Monoamine Neurotransmitters
In summary, there are 3 major drug therapies for treating depression. Each will have its own unique selectivity and mechanism of action, as we just reviewed. They all result in an increase of neurotransmitter in the synaptic cleft, thus strengthening and prolonging each neurotransmitter’s respective post synaptic response
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In terms of monoamine oxidase inhibitors, they selectively target monoamine oxidase and result in an increase in the level of all monoamines in the synaptic cleft.
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Following this, tricyclic antidepressants target the reuptake transporters, specifically for serotonin and norepinephrine, resulting in their increase in the synaptic cleft.
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Finally, the selective serotonin reuptake inhibitors are selective to serotonin reuptake transporters and only result in an increase of serotonin in the synaptic cleft.

Slide 8: Non-specific Effects
Before concluding, it’s important to note that there can be many potential associated problems of antidepressants due to nonspecific drug effects in the body. This is due to the route of administration of these drug classes. When a drug is taken orally in pill form, it must enter the bloodstream via the gastrointestinal track, where it is then free to diffuse throughout the entire body, including the brain, which is where the desired target is in this case for depression. If we look at these 3 drug classes, they each have specific side effects associated with them.
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The first being monoamine oxidase inhibitors, which interact with many foods and drugs, specifically over the counter drugs, which can cause dangerous increases in BP.
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Tricyclic antidepressants also have effects on other neurotransmitters, such as acetylcholine and histamine signalling pathways, leading to dry mouth, irritability, confusion, and constipation.
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And then finally, the selective serotonin reuptake inhibitors can produce side effects like agitation, insomnia, nausea, and difficulty achieving orgasm.

Slide 9: Biological Treatments
That concludes this tricky topic looking at biological treatments of depression.

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Appendix: Tricky Topic Transcripts by Edited by Leanne Stevens is licensed under a Creative Commons Attribution 4.0 International License, except where otherwise noted.

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