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Effects of axon diameter and myelination

Created by Matthew Barry Jensen.

Video transcript

In this video, I want to talk about the effects of axon diameter and myelination because it turns out that larger diameter axons conduct action potentials faster than smaller diameter axons. And axons with a myelin sheath on them also conduct action potentials faster. So first let's consider the diameter of an axon and how that affects the speed of action potential conduction. An axon with a larger diameter offers less resistance to the movement of ions down the axon, causing ions to move faster down the axon and causing the action potential to be conducted faster. Let me show you the way I think about this by just considering a single sodium ion that's entering an axon through a voltage-gated sodium channel. So we'll say we just have a single sodium ion in here we're going to look at, even though there's many sodium ions flowing in through these voltage-gated sodium channels. And let's consider this for both-- the large diameter axon and the small diameter axon. Here's our sodium ion in the large diameter axon. Now, both of these sodium ions, once they're inside the axon, could move in, really, an infinity of directions. They could kind of go in any direction and any degree of direction so that there's an infinity of pathways these ions could travel. Now, if they happened to travel backward in the axon, back toward the soma, or if they happen to travel perpendicular to the long axis of the axon, that won't really contribute much to the action potential other than the effects they'll have on the other sodium ions that are coming in. But if they're heading in any of these directions down the length of the axon, that's going to contribute to moving the action potential down the axon. And the same is going to be true for this sodium ion in the small diameter axon. It could go in an infinity of directions as well, just like in a larger diameter axon. But now let's consider the obstacles to this sodium ion moving down the axon. First, there's the membrane of the axon. And then there are all sorts of structures in the cytoplasm of the axon, such as vesicles or large proteins. And then, there are filaments, and there are tubules. And there are all sorts of structures in the cytoplasm that would pose an obstacle to the movement of this sodium ion. And the concentration of these obstacles would be the same in the smaller diameter axon. But of course, there's less cytoplasm. So there would be fewer of these obstacles, but the same number for any given volume of cytoplasm. So if we consider this to represent the obstacles in the way of these sodium ions moving down the axon, what we see is that there are fewer potential pathways for the sodium ion to move down the axon in the smaller diameter axon before it runs into something in a fairly short distance. So let's say this sodium ion heads this way. That gets it a pretty good ways until it collides into the axon membrane. Or if it goes this way, it also gets it a pretty good ways until it collides with the cell membrane. But if it heads this way, it collides into one of these cytoplasmic structures pretty quickly. Or if it heads in any of these directions, it runs in the axon membrane very quickly. Now, if we compare that to the sodium ion in the large diameter axon, it has more potential pathways to travel before it collides into something. I mean, it certainly has the probability to collide into things in a pretty short distance. But there's a higher probability that it will travel a farther distance at a faster speed because there are just so many more pathways that it can take to make it a farther distance before it collides into something, so that for each individual sodium ion, the probability is higher that it will travel faster over a longer distance than the probability of this sodium ion in the smaller diameter axon. And then when you consider that many, many sodium ions are coming in and you average all those average speeds together, it's going to turn out that, in the larger diameter axon, the ions are going to move faster on average down the axon because they have more potential pathways to travel before colliding into things. And since the speed of action potential conduction is related to the average speed of ions moving down the length of the axon, then action potentials will be conducted faster down a larger diameter axon than down a smaller diameter axon. At least this is the way I like to think about it. But now let's consider the other thing that really speeds up the conduction of action potentials down axons, which is the presence of a myelin sheath around the axon. The speed of action potential conduction is faster in myelinated axons, like I've drawn here with the myelin sheath in yellow, because the capacitance of the membrane is reduced in the myelinated segments, which decreases the number of ions and the time needed to change the membrane potential in these areas. In this context, the word "capacitance" refers to the number of ions that can be stored in the layers on both sides of the membrane at any given membrane potential, because the membrane potential reflects the strength of the charge separation for any particular charge carrier, like a single cation or a single anion. But the total number of charges along the membrane is the "capacitance" of the membrane, a word derived from the same word as "capacity" or the amount of charge that can be stored. One of the principles of a capacitor like the cell membrane is that the closer the charges are to each other, the more charges can be stored on both sides of the capacitor. The way I like to think about that for this is that at the nodes of Ranvier, there's only the normal thickness of the cell membrane, which is relatively thin, so that an anion in the layer against the inside of the membrane is strongly attracted to a cation in the layer on the outside of the membrane. Because they're very close to each other, they're attracting each other very strongly. And because this attraction is so strong, it's able to overcome the repulsion that the like charges feel to each other on either side of the membrane. So all these positive charges-- these cations-- repel each other because like charges repel. But with this very small distance between the opposite charges on the other side of the membrane, this strong attraction overcomes the repulsion that the like charges are feeling on either side of the membrane so that on the thin membrane at the nodes of Ranvier, you can pack in lots of charges. You can pack lots of anions on the layer along the inside and cations in the layer along the outside, at least at the resting potential when it's more negative inside than outside. But the myelin sheath you can think of, really, as making the membrane much, much thicker because the myelin sheath is just membrane that's wrapped around the neuron membrane many, many, many times. So now you have a really thick membrane. So in terms of a capacitor, the distance is now much greater between the opposite charged ions on either side of the myelin sheath membrane. So while they're still attracting each other-- so there will be a cation out here and an anion right here-- and they are still attracting each other. They're trying to pull toward each other across the membrane that won't let them pass. But the strength of this attraction is much less because the distance is much farther between these ions so that now you can put less like charges on the same side of the membrane from each other because there's less of an attraction across the membrane to make up for the repulsion that these like charges are feeling toward each other. They want to move as far away from each other as they can, and so they're spread out much farther. You can store less charges or less ions along both sides of the membrane because the distance between the opposite charges is farther away. So in a myelinated axon like this, there will be this alternation at the nods of Ranvier, which is high-capacitance. There will be lots of charges. And in the myelinated segments, which is low capacitance, there will be less charges. For unmyelinated axons, they're basically all just like the nodes of Ranvier. They're high-capacitance, so they store lots of charges on both sides of the membrane. Now consider when the action potential starts and this voltage-gated sodium channel opens, sodium will flow into the axon, bringing positive charges inside, so this area of the membrane is going to depolarize. And to do so, some of these negative charges are going to need to leave the inside of the membrane and mix in with the rest of the ions in the cytoplasm. And on the outside, some of these charges will have to leave and mix in with the ions in the interstitial fluid. And this will take a little time. And it'll take more time here on the high-capacitance membrane at the nodes of Ranvier, or the trigger zone, than it will here in the myelinated segments just because there are less charges that have to move off the membrane to change the membrane potential. So because fewer ions and less time is needed to discharge or depolarize the membrane in the myelinated segments, which has a lower capacitance, or to recharge the membrane or repolarize the membrane, when potassium starts flowing out during the falling phase of the action potential, the action potential is able to travel faster through these myelinated segments than it can through the nodes of Ranvier, which is why we see slower conduction of the action potential through the nodes of Ranvier than through the myelinated segments, which we call "saltatory conduction," where it looks like the action potential is jumping from node to node. Myelination also decreases the membrane permeability to ions so that fewer ions in total cross the membrane during an action potential. Therefore, fewer ions in total need to recross the membrane after the action potential through the sodium potassium pump that's going to be pumping back out all the sodium ions that came in through the voltage-gated sodium channels and pumping back in all the potassium ions that left during the action potential. And since this process uses energy, myelination increases the efficiency of action potential conduction in terms of the energy needed to maintain these ion concentrations after action potentials. Myelinated axons have most of their voltage-gated ion channels at the nodes of Ranvier, so that while an action potential is conducted faster through a myelinated segment, it actually does decrease in size a little bit as it's going along. The nodes of Ranvier, therefore, are necessary to regenerate the full size of the action potential so that it can continue all the way down the axon.