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  University of Idaho
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  Psychology Dept.
  University of Idaho
  Design - P&D

Hello everyone and welcome back. In our past section we discussed the brain and all of its major structures. In this section we begin discussing neurons.

Let's begin by going to slide two. As we see here, slide two is a diagram of all the different structures that make up a nerve cell. As we can see, there is a wide variety of different structures.

The first of these (as we see in slide three) is called the Soma or the cell body. This is where the cell metabolism takes place. It also has places where it can receive information from other nerve cells which are called postsynaptic elements. It contains a wide variety of different structures that go along with metabolism, such as, mitochondria, endoplasmic reticulum, and a variety of others. For this class they are not really all that important but they are important in other classes that relate to pharmacology and physiology. So, you will probably see these in the future.

In slide four we begin to show information related to axons. Axons are structures that send information to other nerve cells and they have a wide variety of different structures.

The first of these is shown on slide five which is called the axon hillock. The axon hillock is located at the base of the axon. This is generally where the nerve cell decides if it is going to send a signal (called the action potential) to another nerve cell.

The next part of the axon, as we can see in slide six is the body of the axon. This structure can branch into multiple branches and each of these branches is called the collateral. Ultimately the branches continue to branch into smaller and smaller branches. At the final end branching these are called Teleodendria.

At the end of each one of these teleodendria (as shown in slide seven) there is a little knob. These little knobs are called terminal buttons, terminal boutons, and a wide variety of other names. However, the most correct name in the literature today is what we call the presynaptic element.

The presynaptic element as we can see in slide eight contains a wide variety of structures. The first of these is called the synaptic vesicles. Synaptic vesicles are basically sacks; and these sacks contain chemicals called neurotransmitters. There is also a membrane in the presynaptic element. This membrane contains two major groups of structures; autoreceptors and reuptake channels and we will talk about these a little bit later. Presynaptic elements also have receptors from other neurons, and they also contain calcium channels and other structures that we are not going to talk about here.

A picture of a presynaptic element is shown on slide nine and you can see where all of these structures are located.

Axons can be identified as one of two types. The first of these is shown on slide ten. These are called myelinated axons. Myelin is basically a fatty covering that covers the axon. What it does is help the speed of the action potential. The more myelin there is, the faster the speed of the action potential.

The other type of axons (as we see in slide eleven) are non-myelinated axons. These are axons that do not have any myelin. They are slower than myelinated axons. However the fatter the axon is the faster the action potential goes. These are all the structures we need to know about on the axon.

The other major sets of structures that come off the Soma are the dendrites. First of all (as we see in slide twelve); some neurons do not contain dendrites and only have soma's or axons. Generally, dendrites only receive information. They also contain several major substructures. The most important of these is the post synaptic element. The post synaptic element like the presynaptic element has a membrane and this is called the post synaptic membrane. It also has receptor sites which receive the neurotransmitters that come from the presynaptic element.

So in general, as we can see in slide thirteen, dendrites and soma's can receive information and both contain a post synaptic element.

You can see on slide fourteen a diagram of the post synaptic element, receptor sites, different ion channels and the membrane.

There is a space between the presynaptic element and the post synaptic element. That is, the presynaptic element and the post synaptic elements do not touch each other directly. This space is what we call the synaptic cleft. All it is is a space between the two different structures.

So, how do neurons work? As we can see in slide sixteen, neurons work based on the concentration gradients of four different ions; Sodium, Potassium, Chloride, and structures located inside the axon collectively called Anions. Now, sodium and potassium are positively charged and they are balanced out by chloride and the anions.

As we can see in slide seventeen, normally some sodium naturally leaks into the inside of the axon. But cells do not like sodium and they have pumps inside their structures to remove the sodium. These pumps are called sodium-potassium pumps. They move sodium to the outside of the neuron.

The inside of the axons as we see in slide eighteen have lots of potassium and anions. Generally, when compared to the outside of the axon they are negatively charged. The outside of the axon has lots of sodium and chloride and generally is positively charged. So when an axon is at rest, the outside of the axon is positively charged and the inside is negatively charged.

So what about action potentials? Action potentials, as we see in slide nineteen, occur because voltage-gated channels, which are different than other types of channels, open. And when they open, there is a large and rapid amount of sodium influx to the inside of the axon. As a result of this sodium coming in, the inside of the axon becomes more positive than the outside. There name for this process is called depolarization.

A diagram of this is shown on slide twenty and the process of an action potential. You can follow along with each of the numbers to get an idea of how it works.

A breakdown of this process is shown in slides twenty-one and twenty-two. Let's start with slide twenty one. As we can see, first of all, stimulation begins. As a result potassium begins to leave by passive channels inside the axon. Sodium begins to enter by passive channels. This causes a basic change in concentration gradients. How much change depends on the strength of the stimulus, how often it occurs, etc. Ultimately if this depolarization reaches fifteen millivolts, voltage-gated sodium channels will open and sodium will then enter to the inside of the axon. And this is what we call sodium influx. As soon as this begins, sodium and potassium pumps begin to try to pump the sodium back out and they also bring potassium back in. Because there is so much sodium coming through the inside these pumps are overwhelmed. Potassium will also, as we can see here, pass through these channels. But then, again, there is a problem because there is so much sodium coming in.

Finally, about a half second after the sodium voltage gated channels open, potassium voltage gated channels will begin to open as well. As a result of that (as we can see in slide twenty-two), potassium begins to leave. Basically it is pushed out because like charges repel. As we get to number five we see that the sodium channel finally closes and the action potential begins to fall. Finally at number six, the potassium gate finally closes. Potassium is still leaving by passive channels and sodium is being pumped out by the sodium-potassium pump. As a result of both of these things, the action potential continues to fall until it falls lower than it actually was in the beginning. This is called a negative undershoot and the signal it begins to drop down a lot. Ultimately, at the bottom of this undershoot, another set of channels begin to open. These are called calcium channels. There still is not enough potassium so calcium continues to enter. This is called calcium influx. Finally at number nine enough potassium has entered so the calcium channels finally begin to close. At number ten the calcium channel finally is closed and the process repeats itself.

So for a review (as we see in slide twenty-three), when a stimulus enters a receptor it causes a change in polarity. This causes a change in concentration gradients. It initially allows sodium to enter the inside of the axon in small amounts. When it travels to the hillock, and if the hillock polarizes fifteen milli-volts you get an action potential. Now, if the charge isn’t strong enough, say its thirteen milli-volts, and then the signal will actually stop.

Once there is enough sodium inside and there is depolarization at fifteen milli-volts, it causes the sodium gates inside the axon to open, and you get sodium influx. So the inside of the axon goes from negative to positive on the inside of the axon. This goes down the axon like a wave. After the sodium enters, the pumps begin to turn on and begin to remove the sodium and that also goes down like a wave.

So in essence what you have is two waves going down the axon. The first of which is sodium entering the axon and the second wave is the sodium being pumped out. Regardless of all the procedures involved, ultimately the result is the negative undershoot and this is the most important aspect.

So what happens when the action potential reaches the presynaptic element? As we can see in slide twenty-six, it causes calcium to enter the presynaptic element. And when calcium enters it binds with the presynaptic membrane. This causes the neurotransmitter to be released into the synaptic cleft. The neurotransmitter then crosses the synaptic cleft and binds on the receptors of the post synaptic element on either a dendrite or a soma. This causes a small electrical change and the process repeats itself.

So now we have all this neurotransmitter on the receptor sites, how do you get the neurotransmitter off? Well, as we see in slide twenty-seven, the neurotransmitter is removed in two ways. The first way is that it is degraded by enzymes made by glial cells or within the post synaptic membrane. The second way and one of the most important ways when we talk about drugs is that it is reabsorbed back into the presynaptic element.

As we can see in slide twenty-eight drugs will have a wide variety of different ways to impact on the axon. First of all, some drugs impact the entire neuron, such as alcohol. Other drugs target the presynaptic element, such as cocaine and methamphetamine. A third group of drugs (such as opiates) target the postsynaptic element. Finally, some specific drugs target specific receptor sites located on receptors (such as with barbiturates or benzodiazepines such as valium). The key for all these drugs is alcohol because alcohol targets everything within the neuron, the axon, the dendrite, and all the elements. So it is very, very powerful and has a wide variety of different effects.

Alcohol as we will see later first alters the lipid bilayer of a neuron, that is, it slows the ion flow. This will ultimately reduce the height of the action potential, reduce calcium influx, and as a result, fewer neurotransmitters are released. This causes less stimulation on the post synaptic element and less depolarization in the next neuron. That is, it does not become as positive. And as a result there are fewer action potentials that occur in the next neuron.

Some drugs as we see in slide thirty block the reabsorption of neurotransmitters and as a result of that the neurotransmitter remains on the post synaptic elements longer period of time plus you get more action potentials. A classic example of this is cocaine.

Another major aspect as we see in slide thirty-one is that some drugs actually block neurotransmitters from binding on the binding site on the receptor. As a result of that you get less depolarization, fewer action potentials, and depending on the brain area where this is occurring (such as on the medulla) it can cause death, or temporary memory loss such as in the hippocampus. A classic example of drugs that do this are the opiates.

So in conclusion, when one talks about looking at different types of drugs and how they work one really has to focus on the neuron itself. As a result, we have discovered lots and lots of things about how drugs work at particular receptor sites. Further, it has really increased our understanding about how drugs work both positively and negatively.

In our next section we are going to look at how drugs impact a variety of different brain structures from an overview. So, until then, we hope you have yourself a great day and we look forward to talking with you soon.