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

Basically the process of an action potential begins with some kind of stimulation. As a result, potassium begins to leave by passive channels and sodium begins to enter by passive channels. As a result of that, you begin to get a change in the amount of concentration on the inside in relation to the outside. So again, what you’re doing is getting some kind of depolarization. The depolarization is going to depend upon the length of the dendrite, the strength of the stimulus, temporal summation, length constant, and a variety of other things. Ultimately all of this process begins depolarization. Now as we talked about in the last section, if depolarization reaches 15 millivolts (mv) voltage-gated sodium channels begin to open very rapidly. What you get is a major amount of sodium influx to the inside of this axon. As a result you’re going to start to see a rise in the potential that you saw in slide two, so the height of the curve is going to go up.

As we can see at number four, we start to get sodium-potassium pump starting. These begin to remove the sodium and bring in potassium. As you can see, they’re starting very, very rapidly after depolarization has occurred and the action potential is starting to rise. But, because so much sodium is flooding to the inside, these systems are overwhelmed. What you’re going to do is remove three sodium ions for every two potassium ions that you bring back in.

Potassium, at the same time as number four, is also leaving through passive channels due to the electrostatic pressure that’s on the inside of this axon. Remember it’s becoming more positive. As we get it more positive, the positive charges repel because there’s so much sodium. Thus, potassium begins to leave. As the action potential continues to be polarized and become more positive, these voltage-gated channels begin to open (about a half a millisecond after the sodium voltage gated channels open). So, as we see in slide five at number five, at the very height of the action potential, the sodium is at equilibrium and all the sodium is equal on the inside and the outside. As a consequence, that voltage-gated active channel is still open but the voltage-gated inactive channel finally closes. So no more sodium is going to be entering to the inside of the axon.

Because of the action of the sodium potassium pumps and the fact that potassium is leaving by active and passive channels , the action potential begins to fall. This decrease continues to fall until we get to number six. At number six what we see is that the potassium inactive gate finally closes. Now, you’re still getting potassium leaving through the passive channels, and you’re still getting sodium leaving by the sodium-potassium pump, but the action potential continues to fall because the sodium leaving and that there’s not very much potassium back on the inside of the axon.
Now we continue on and ultimately get a negative undershoot from the original resting state. At number seven, what begins to happen is that it becomes so negative that the calcium voltage-gated channels begin to open. You still don’t have enough potassium, so what you have is a large amount of calcium influx. Finally the potassium comes in so much that the calcium inactive channel begins to close. Finally it closes completely at number ten and the process repeats itself.

So, in general, in a review here, when a stimulus alters a receptor, it’s going to cause a change in polarity (it changes concentration gradients). Sodium enters first of all and depolarizes the neuron and then in large amounts it continues down to the axon hillock. If it depolarizes 15mv we get an action potential. And again, if the charge isn’t strong enough, nothing happens and the signal stops. And as we can see in slide seven, it continues on. If the sodium channel is open, you get the sodium influx, the axon then goes from negative to positive on the inside and is going to go down like the axon like a wave. After the sodium enters and the potassium pumps begin to turn on and removes the potassium, that system also goes down the axon like a wave. So in essence you have two waves going down the axon; one where sodium is entering the axon and then one where sodium is being pumped out. The ultimate result of this and the most important part is the negative undershoot that’s at the bottom of that action potential curve.

So what happens, then, when this axon reaches the pre-synaptic element, what occurs. Well as we can see in slide 10, it causes calcium to enter the pre-synaptic element. Calcium causes the synaptic vesicles to move down protein filaments. Ultimately these filaments and vesicles bind at the pre-synaptic membrane. So what’s going to happen is that if you get no calcium, you get no efflux or release of neurotransmitter. (There’s a couple of chemicals that will block this and one of those, as we see here, is botulism toxin).

So, ultimately what’s going to happen is that the neurotransmitter is going to be released into the synaptic cleft. The neurotransmitter is then going to cross the cleft and bind on the receptors of the postsynaptic element. As a result, you get a small amount of depolarization and the process repeats itself. This is called the excitatory postsynaptic potential and we’ll talk about this again in a little bit.

Now there’s one other concept that goes along with all of this. That is the concept of saltatory conduction. We’ve been talking about the process of the sodium coming in and the potassium leaving primarily within a nonmyelinated axon. That is, an axon that doesn’t have any kind of fatty myelin surrounding it. However, what happens in a lot of axons is that we have myelin around it. As a result, there’s fatty covering with kind of small spaces between these pieces of myelin. Here is where the constantly salvatory conduction is important. As we see in slide 12, when you get the action potentials traveling down the axon, it depolarizes the sodium voltage-gated channel and the one that’s right next to it. As a consequence if we’re doing this in a nonmyelinated axon the process takes a long time So, what would happen if we were able to skip a bunch of these places? That is where myelin comes in. What myelin does is allow the action potential to jump from one Node of Ranvier to another Node of Ranvier. So, the action potential is going to depolarize the next sodium voltage gated channel at the next Node of Ranvier. As a consequence, the skipping or salvatory conduction requires a lot less work and increases the speed of the action potential even in small axons. So, myelin is extremely, extremely important.

One final set of concepts in relation to the action potentials shown in the summary page. First, the action potential as we’ve seen is an all or none event. It also has a fixed height (basically the equilibrium gradient that we have with sodium), which is a positive 55mv. It also has a very specific velocity that we can measure in meters per second. That velocity depends on two variables; myelin and the amount of it and the axon diameter. Finally the action potential has what we call an absolute refractory period in which stimulation will not produce an action potential. Even if you artificially stimulate it, you rarely get an action potential to occur in a refractory period. When you do that experimentally, the amount of charge difference is incredibly large.
So, in general, the action potential is extremely, extremely important for us. What it does is basically cause neurotransmitters to be released.

In the next section what we’re going to talk about is what happens with these neurotransmitters and the neuro-chemical processes that go along with it. So until that time, we hope that you are studying hard and we will be looking forward to talking with you soon.