July 27, 2023

Module 2: The Biological Level

Read the all module 2 and at the end of the pdf fill out the review and reflect part. and there is some questions in the pdf we need to answer them as well.

Module2.pdf

Module 2

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Module 2: The Biological Level Tuesday, July 11 – Monday, July 17

Required

Reading/Viewing:

Principles of Psychology, Chapters 3–4

(Pages 64–102; 122–145; 165–184)

Module 2 online content

interface (2011, October 16). Stress: Portrait of a

Killer. A National Geographic Documentary (2008)

[Video]. YouTube.

Discussions: Module 2 Discussion

Initial responses due Friday, July 14, 9:00 AM

Two peer response due Monday, July 17, 9:00

AM ET

Leader response due Wednesday, July 19, 9:00

AM ET

Assignments: Film Response Worksheet 1 due Tuesday, July 18,

5:00 PM ET

Live Classrooms: Tuesday, July 11, 7:30–9:00 PM ET

Activity: Complete Module 2 Review and Reflect, due

Tuesday, July 18, 11:59 PM ET

Welcome to Module 2

cas_ps101_19_su2_mtompson_mod2 video cannot be displayed

here

The story of Phineas Gage shows us which of the following?

The importance of certain brain regions in regulating social behavior. That a minor accident can lead to enormous problems in behavior. That damage to the frontal regions of the brain leads to problems with movement and speech.

CHECK ANSWER

VIDEO FOLLOW-UP

Learning Objectives

1. List methods for studying the brain and specify the advantages and disadvantages of each.

2. Describe how brain cells function.

3. List major brain regions and their functions.

4. Describe the difference between “sensation” and “perception.”

5. Describe the pathway through which light travels from the eye to the brain, allowing us to see images.

6. List cues that we use to determine depth perception.

Brain

Introduction

Think back to the introductory lecture when I introduced the “levels of analysis.” Today we are going to focus on the biological level. We are going to

focus on the brain and how it underlies human behavior.

In talking about the brain, it is important to distinguish between structure and function. The brain’s structure is how it is built, what it looks like, and

what parts are included.

Its function is how those these parts work together to get the job done. Think of it like a car. The car’s structure includes its parts—spark plugs,

braking system, etc. The car’s function is how, when you start it up, all the parts work together to move it forward.

We are going to be focusing in this module on both structure and function.

Methods for Studying the Brain

But first, let’s look at the big picture…how do we study the brain? There are many techniques, each with advantages and disadvantages. I’m going to

review several, but this is certainly not a comprehensive or exhaustive list; more are being developed!

Autopsy

Here brains can be examined after death.

As an example, Boston University has the largest repository of brain tissue in the world focused on studying CTE. What is CTE? Chronic Traumatic

Encephalopathy.

You may be aware that CTE has been of intense interest for some time now because of strong evidence that sports injuries, particularly those

occurring on the football field, may lead to CTE.

Advantages: Autopsies allow researchers to examine real human tissue and can tell us a lot about the structure of the brain.

Disadvantages: The brain is dead, so we can’t see it at work. It’s like looking at a car that no longer runs. Although we can learn a lot about

structure, we can’t learn much about function.

Animal Models

We are mammals; other mammals’ biological processes are similar.

As an example, much has been learned by administering drugs (e.g., cocaine) to rats to examine their impact on behavior and on brain structure

(after “sacrificing” the rat). As another example, in animal models the brain can be damaged in a very specific area (a specific lesion, we call it),

and the impact of the damage can be studied.

Advantages: Within certain ethical guidelines covering animal research, we can still conduct studies that we could not do with humans.

Disadvantages: Sometimes it is hard to generalize to humans. We can’t easily replicate complex cognitive phenomena. For example, rats don’t

learn to read, so we can’t look at how reading is learned in rats!!

Testing Folks with Brain Damage

These are “experiments of nature.” By understanding what happens when something goes wrong, we can learn about how the brain actually

works.

As an example, let’s say that a person has very specific damage in a certain area of the brain (maybe as a result of a stroke—a bleed in the brain).

By carefully testing them we can learn so much about the impact of damage to that region on the individual’s behavior. We will talk a lot more

about this when we talk about memory. Let me briefly describe the case of H.M. (so called to disguise his identity). H.M. had severe epilepsy (a

seizure disorder) and had brain surgery to treat it; the doctors removed a particular region on both sides of his brain with the hope that it would

improve his seizures. Unfortunately, very unfortunately, when he awoke he was no longer able to form ANY new memories about his life. Crazy as

this sounds, he was able to have interactions with people daily and yet have to be introduced to them anew every day. Although he could

remember things that happened prior to the surgery, no new memories (events after the surgery) could form. Sound horrifying? H.M. was tested

extensively over the years, and this research greatly increased knowledge of the role of specific brain regions in forming new memories.

Advantages: We can do these studies ethically and learn much.

Disadvantages: The damage may not be as specific as we would need it to be to really understand fully the function of small areas (it is not a

controlled experiment). There may be other (undetectable) damage influencing what is happening. The brain also undergoes changes AFTER

damage; our brain may reorganize in some ways to compensate. The problems that lead to the damage in the first place (in H.M., seizures) may

have changed the brain in some ways.

Computerized tomography (CT) scanning builds up a picture of the brain based on the differential absorption of X-rays.

Advantages: CT is relatively cheap and quick and is useful in revealing the gross features of the brain. For this reason it can be used in medicine

to diagnose tumors, aneurysms, and other phenomenon.

Disadvantages: CT has poor resolution and details cannot be seen clearly.

EEG

Electroencephalography (EEG) measures brain electrical activity by recording from electrodes placed on the scalp. The signal represents the

electrical output from what we call the cortex of the brain.

Example: EEG has been used to study the activity of the brain during sleep; we will talk about this a lot more later on in this course. It can also be

done over extended periods of time. For example, in diagnosing seizure disorders, portable EEG equipment allows data on brain activity to be

collected over a series of days, not just minutes or hours.

Advantages: EEG has good temporal (in time or when) resolution (that is, it is capable of detecting changes in electrical activity in the brain on a

millisecond-level), and it is one of the few techniques with such good temporal resolution.

Disadvantages: It doesn’t have good spatial (where) resolution. So while we can determine when a change in activity took place, we cannot

determine exactly where in the brain the change happened.

PET

Positron Emission Tomography (PET) uses trace amounts of short-lived radioactive material to map functional processes in the brain. When the

material undergoes radioactive decay a positron is emitted, which can be picked up by the detector. Areas of high radioactivity are associated with

brain activity. So you can see how specific chemical substances change during certain tasks.

Example: PET has been used to look at certain kinds of deposits in Alzheimer’s disease—a primary cause of dementia. It’s helped us to

understand the process of how this disease works.

Advantages: PET can detect cellular level metabolic changes, so it is very specific. Particular radioactive tracers can be used to look at specific

chemicals.

Disadvantages: Many folks may not be comfortable with having an injection of a radioactive tracer. It’s also expensive.

fMRI

In fMRI, a very powerful magnet is used to detect changes in blood oxygenation and flow that occur in response to neural activity. Active brain

areas consume more oxygen leading to increased blood flow. FMRI can be used to produce activation maps showing which parts of the brain are

active during a particular mental process (for example, reading, listening to music, watching images on a screen).

Example: We can look at which regions are active during certain tasks. Researchers at Harvard actually wanted to look at how individuals respond

to parental criticism! They obtained audio recordings of individual subjects’ mothers criticizing them. The researchers then played the recordings

to the subjects while they were in the fMRI scanner and examined which brain regions were active! Pretty interesting!

Advantages: FMRI can assess changes during specific tasks (i.e., memory tasks, watching videos, making ratings), because it has pretty good

temporal resolution—the brains response is close in time to the event.

Disadvantages: FMRI is very sensitive to movement; the study subject has to stay very still in the scanner!

This sensitivity to movement makes it hard to do fMRI with children, as they aren’t so good at staying still. That said, strategies have been

developed to help kids feel comfortable and to get good fMRI data. It’s also a little disconcerting to be in the scanner, as it is a pretty tight space.

If you have claustrophobia (a fear of closed-in spaces), fMRI is pretty distressing! It’s also expensive.

Now that we’ve reviewed some of the major techniques for studying the brain, let’s focus on some of what we know. We are going to focus on structure

and function by examining individual neurons (nerve cells) and neuroanatomy (the major structures of the brain).

Brain Cells and Their Function

Let’s focus on neurons. The average brain has about 100 billion neurons! In addition, there are many other cells that support and protect your brain.

So, what are some of the major parts of the neuron. First, on the left side of the image are the dendrites. Remember that there are other neurons

further to the left and right (this is just one cell). The dendrites take in information from the adjacent cells. That information is merged in the cell

body, which then sends an electrical signal down the axon. The axon is coated by a substance called myelin. Myelin speeds the rate of electrical

transmission down the axon. Interestingly, there is much less myelin on the axons of the brain during infancy; over the first two years of life, neuronal

axons are acquiring myelin, making transmission of messages much faster. The child rapidly becomes more capable of a variety of activities and

responses. We also see lots of myelination during the adolescent years—a period of rapid brain development. During adolescence, neuronal

transmission becomes much faster and more efficient—adolescents are becoming better and faster thinkers! We will get back to this.

Back to the electrical signal coming down the axon: As the axon comes to an end, it begins to branch out. When the electrical signal gets to the end of

these axon branches, the signal needs to get to the next cell. This is where the process changes from an electrical one to a chemical one. This

is why we refer to neural transmission as an electro-chemical process. The terminal endings do not actually touch the dendrites of the next cell.

There is a gap between the terminal ending of the axon and the dendrite of the next cell, and we refer to this tiny gap as the synapse. So here’s

what’s happening with synaptic transmission, that is, transmission across that gap or synapse. Within each axon terminal ending there are tiny

pockets of a chemical substance or neurotransmitter that is produced by the cell; these tiny pockets that store the neurotransmitters are

called vesicles. The nerve impulse stimulates these vesicles to move to the end of the terminal button and to release their contents into the

synapse. These neurotransmitters then attach to specific receptor sites on the dendrite of the next cell—we call this next cell the postsynaptic

neuron. Some neurotransmitters are excitatory—tthey increase the likelihood that the next neuron will fire (send an electical signal down its axon);

some are inhibitory—they decrease the likelihood that the next neuron will fire. It is the sum of all of the inputs that determines what will happen (to

fire or not to fire, that is the question!).

Here is a different view of the synaptic transmission.

So, what happens to the neurotransmitter substance after it is released into the synapse? There’s leftover in the synapse; what happened to it?

Well, two things can happen. First is a process we call reuptake. In reuptake the neurotransmitter substance is taken back into the cell from which it

was originally released. It can then be used again in the future. I think we can consider this the brain using recycling. Second is a process

called degradation. Your brain is a small but efficient chemical factory, producing many substances. In addition to neurotransmitters, it also produces

a number of enzymes. Some of these enzymes are involved in the process of degradation, and they essentially come in and "clean up" the leftover

neurotransmitter. When I think of this, I imagine them as little street sweepers, getting rid of the old junk and mess.

Implications: Neurons, Medical Disorders, and Medical Treatments

So why is all this important? It’s important at the level of basic and applied science.

I think the best approach to thinking about this question is to use examples. A couple of interesting examples help us to explain some behavioral

disorders.

1. How many of you know what multiple sclerosis or MS is? MS is an autoimmune disorder in which the immune system attacks myelin on

neuronal axons. The myelin is broken down, and this impacts the rate of neural transmission. Individuals with MS experience a range of

symptoms, including changes in vision and difficulties with motor activities. The effects of MS will vary depending on which neuronal axons are

most affected, and the symptoms of MS can vary between individuals.

2. As another example, too much or too little neurotransmitter can cause problems. The neurotransmitter substance dopamine is involved in a

number of important functions. You may have heard about the pleasure center of the brain, which is a dopamine-rich area in the midbrain (we will

talk about the midbrain a little bit later). Stimulation of dopamine neurons in this part of the brain leads to feelings of pleasure. In Parkinson’s

disease, we see the death of dopamine cells in a particular part of the midbrain called the nigra striatum. The nigra striatum is essential in

movement. One of the main symptoms we see in Parkinson’s disease is difficulties with movement. The death of those dopamine cells underlies

the symptoms we see in Parkinson’s disease.

3. Let’s focus a little bit more on dopamine. Let me take a little bit of a side trip. How many of you have heard of schizophrenia? Schizophrenia is

what many people think of when they think of “mental illness.” Indeed, schizophrenia is a severe mental illness in which individuals experience

perceptual distortions, including hallucinations, and may develop delusions, which are odd beliefs not based in fact, including severe paranoia. One

of the major theories about schizophrenia is known as the dopamine hypothesis. This is the idea that too much dopamine neurotransmitter in

certain brain regions may lead to some of the symptoms that we see in schizophrenia.

So by understanding something about neurons and neurotransmitter substances we can understand something about neurological and behavioral

disorders. We can also understand how some drugs work that affect behavior. I’m going to talk about the impact of some drugs that are used to treat

psychiatric and neurological disorders. I want you to remember something. When you take a drug, you generally take it orally, that is, you swallow a

pill. However, when taken orally, a medication goes to the places you want it to go to have the effect you’re looking for, and it also goes to places where

you don’t want it, causing side effects. For example, let’s say that you have a lung infection and so you take an antibiotic to treat it. That antibiotic

goes through your bloodstream and hopefully kills the infection in your lungs. At the same time, it may go into your digestive track and kill some

bacteria in your gut that are actually pretty useful. Sometimes people get stomach and digestive problems as a side-effect when they are taking

antibiotics.

Here is another example. Antipsychotic drugs have been used to treat schizophrenia. Most antipsychotic drugs are dopamine antagonists. What does

this mean? This means that they reduce dopamine. They generally do this by blocking the postsynaptic neuron so that dopamine cannot have its effect

to the same degree. By reducing dopamine, these antipsychotic drugs can have a powerful impact on behavior. They are frequently used in the

treatment of schizophrenia to reduce the hallucinations and delusions of the disorder, and they do so pretty effectively. But there are side effects as

well. This is because they also reduce dopamine in the part of brain called the nigra striatum, and one of the side effects of antipsychotic drugs is that

they can produce Parkinson-like symptoms. If you look at videos of patients in psychiatric wards, you can see some move slowly, they don’t swing their

arms (rather holding them tightly to their sides), and they appear quite still. These are all the Parkinson-like side effects; we say Parkinson-like

because it doesn’t really lead to dopamine cell death, like you would see in Parkinson’s disease, and the symptoms go away if you stop the

antipsychotic drug. It would be great if we could send the medication only where it’s needed and not to places where it’s not needed! This is one of the

great challenges in current drug development efforts.

1. L-Dopa: Now in the case of Parkinson’s disease, there is too little dopamine in the nigra striatum because the cells are dying. It would be good if

we could give people dopamine to treat their Parkinson’s disease; however, dopamine is a large molecule and it does not cross what is called the

blood-brain barrier (a system of microvascular cells that, among other things, protects our brain from toxins). But we can give people something

called L-Dopa, which can cross the blood-brain barrier. L-Dopa is a chemical precursor to dopamine. When given to people with Parkinson’s

disease, it helps them to synthesize dopamine in the brain, and it improves the symptoms of Parkinson’s disease. However, L-Dopa can have some

side effects! Remember, it’s not just going to the nigra striatum; it also ends up in parts of the brain that may be implicated in schizophrenia. So,

for some patients, a side effect of L-Dopa can be the development of hallucinations! Not a good side effect!

2. SSRIs: Another class of drugs that has been developed to treat a range of psychiatric problems, including anxiety and depression, are the

selective serotonin reuptake inhibitors or SSRIs. Serotonin is a neurotransmitter substance that is important in the regulation of mood; low levels

of serotonin have been associated with depression (among other problems). So how do we think that the SSRIs work? Well, they do exactly what

they say they do—inhibit the reuptake of serotonin from the synapse. When reuptake is inhibited, there is more serotonin available in the synapse

to continue to have an impact. I think this can be confusing. Reuptake reduces the amount of serotonin that is available, and by reducing

reuptake, increases the amount of serotonin available. It’s a bit of a double negative: by reducing the reducer, we increase serotonin. It is this

blocking of reuptake that is thought to underlie the antidepressant effect of SSRIs.

3. MAOIs: Let me tell you about another antidepressant medication. These medications are known as MAOIs, which stands for monoamine oxidase

inhibitors. Norepinephrine, along with serotonin, is an important neurotransmitter that is widely distributed in the brain and seems to be

strongly related to depressive disorders. Norepinephrine appears to be reduced in those with severe depression. So what is monoamine oxidase?

Remember how I mentioned that one of the ways that we get rid of leftover neurotransmitter substances in the synapse is through degradation?

Degradation occurs when enzymes come in and “clean up” the remaining neurotransmitter. Well monoamine oxidase is one of those enzymes, and

it specifically “cleans up” norepinephrine. So a monoamine oxidase inhibitor or MAOI will reduce the activity of monoamine oxidase. Again we have

a double negative kind of situation: the MAOI reduces the thing that reduces the norepinephrine (that is the monoamine oxidase). The MAOIs can

be very effective in the treatment of depression; however, they’re not used all that often. Why might this be? Well, people who are taking MAOIs

have to be on a special diet low in tyramine, as the MAOIs make it hard to metabolize tyramine. Ingesting foods high in tyramine, for example red

wine or aged cheese, can be deadly for those taking an MAOI. One thing to remember about depression is that it is associated with thoughts of

suicide and sometimes suicidal behavior. The last thing a doctor wants to do is give the patient a potentially deadly medication.

I hope these examples give you a sense of why it’s important to understand processes involved in neurotransmission. I’ve focused on a few very

“practical” examples, but there many, many more, both basic and applied.

Module 2: The Biological Level

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