© 2010
  University of Idaho
  All rights reserved.
  Psychology Dept.
  University of Idaho
  Design - P&D  CTI

To do this, let’s begin by talking about a couple of concepts. The first concept that I want to talk about is depolarization. In essence, when one depolarizes something, it becomes more positive. And when one hyperpolarizes something, it becomes more negative. So, an example of depolarization would be going from a minus 60 millivolts to a minus 40 millivolts, while hyperpolarization would be going from a minus 60 millivolts to a minus 80 millivolts. That is, one becomes more positive while the other becomes more negative.

So, let’s now talk about electrotonic potentials. These are what also called passive potentials and they have a couple of concepts. The first thing that we talk about when we discuss electrotonic potentials is that they’re detrimental. That is, they decay. The strength of the charge decays over some distance, and the rate of decay depends on a variety of different things. For example, the distance measured from the point of stimulation, the amount of myelin that’s available on an axon, the length of an axon, and the diameter of an axon. There are other variables as well (such as the amount of potassium that’s in the extra cellular space), but we won’t go into that right now.

So let’s take a point of stimulation. And as we can see, this point of stimulation it begins at a minus 70 millivolts. Then, if we go both ways from this point of stimulation, the charge decays as we go farther and farther and farther away. In one case it becomes more positive; in the other case it becomes more negative.

The charges travel in both directions and they decrease in both directions. So as you begin to stimulate something, you get a lot of depolarization or positives changes there. Why? Well, what happens is that potassium begins to move against the membrane, and leaves through process of diffusion. So, if the membrane is very thick, the length of the dissipation increases. From that we can develop a concept and called the length constant. The length constant is the distance along the membrane from the point of stimulation or charge to where the resting potential has dissipated to 37% of the original. So, if you start at rest, at the point of stimulation is 100 millivolts, as we can see in slide seven, the length constant basically goes down to 37% of where it was initially. So, in this case, 37 millivolts. And in slide eight, you see this in a diagram.

Now, in addition to the length constant, there is another concept that we need to talk about. That is the concept called temporal summation. Here instead of having one large stimulus, what we do is present some kind of stimulus every millisecond or so. It might be one, two, or three. That’s why there’s a space there. Once we continue to stimulate that point over time, we begin to see that the axon begins to depolarize. You see this as we walk along the curve in slide nine. The point of stimulation begins and it continues on until it reaches a minus 45 millivolts. Now, again, if it goes 15 millivolts, what happens? Well, we get an action potential. So, why is this all important, why do we get this decrease over time from the initial point of stimulation? Well, it relates to the concept of what we call resistance. Basically, if a membrane is resistant to potassium leaving, it becomes more difficult for the potassium to leave. The speed is again the same, and the potassium leaves through passive channels. So, if you decrease resistance by increasing the diameter of the axon, what you’ll also have is a change in the length constant. This change will also relate to what’s going on with temporal summation. So, how are you going to get an action potential? Well as we can see in slide 12, what you need to do is add and subtract charges. The major concept that you have to remember is that you need to depolarize the membrane 50 millivolts before voltage gated channels open and you get an action potential.

So let’s take a look at some different neurons and different dendrites from different points of stimulation. This begins in slide 13. As we see in slide 13, what we have are four different points, we have point A, point B, point C, and point D. So let’s begin on slide 14 and see what happens. Let’s say that we stimulate point A and we depolarize it 20 millivolts. Well due to the resistance that we have in the dendrite, by the time that charge gets down to the axon hillock, you only have 5 millivolts of depolarization.
So, what about B, or C, or D, or one of the other ones? Well let’s measure point D. So, again we stimulate point D we get a depolarization of 20 millivolts. Well what about the next one, what if we stimulate point B? Well, if we stimulate point B (as we see in slide 16), you only get 8 millivolts. And finally, if you stimulate point C, you depolarize at 20 millivolts, but when you measure it again at the hillock, you get 15 millivolts of depolarization. So let’s kind of run through these in general. As we see in slide 18, when you stimulate A alone, you’ve got nothing, there’s no action potential; B and D alone, you also got nothing. However, if you stimulated C alone, the voltage gated channels open and you got an action potential. Why? Because it was 15 millivolts of change. And, when it depolarized 15 millivolts, voltage-gated sodium channels open.

Well there’s one other concept that we can also do as well. We could add those charges. So, if we add depolarization of A, B, and D, and all the depolarization that goes along with it, the combination of all three of those causes the voltage channels to open, and you get your action potential in the following neuron. So again, what are all those combinations, or what do we need to have which can influence all this? Again, a couple of major concepts. The distance away from the point of stimulation to the hillock will have a major, major role. Also temporal summation will have a role. So the more that fires, the faster it does, the more you’re going to get the depolarization occurring at the hillock.

We also can have inhibitory neurons, so let’s say neuron C was firing and we were getting that charge to the hillock, but because of some inhibitory neuron with an axo-axonic synapse causing it to hyperpolarize, nothing happened because it became more negative. So, what we do is take the combination of all the depolarization from all the different axons and all of the hyperpolarization from other different axons out there. Ultimately if it gets to the hillock and has 15 millivolts of depolarization, you get those voltage gated channels to open. But, ,again, if you don’t get 15 millivolts of depolarization, all those combinations of charges die out, and nothing happens and the next neuron does not fire. So, this is the way that passive potentials work.

In the next section, we’re going to talk about the action potential and how the combination of both is put together. So until then, we hope that you’re enjoying the class and that you’re having yourself a great day. We will be looking forward to talking with you again soon.