Health and medicine
- Neuron resting potential description
- Neuron resting potential mechanism
- Neuron graded potential description
- Neuron graded potential mechanism
- Neuron action potential description
- Neuron action potential mechanism
- Effects of axon diameter and myelination
- Action potential patterns
Created by Matthew Barry Jensen.
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- Is there an equation to represent the relationship between the thickness of the myelin sheath and the efficiency of action potentials?(12 votes)
- Hi ! That’s a very interesting question indeed. The answer is yes, but it’s a bit complicated. If you have some time, I recommend you start by the following articles to have an idea of how scientists worked out the mathematical formalization of the neurophysiology of myelinated nerve fibers.
Goldman L. & Albus J. | Computation of Impulse Conduction in Myelinated Fibers; Theoretical Basis of the Velocity-Diameter Relation (Biophysical Journal, Vol. 8, No. 5, May 1968)
Smith R. & Koles Z. | Myelinated nerve fibers: computed effect of myelin ￼￼￼￼thickness on conduction velocity￼￼ (American Journal of Physiology, Vol. 219, No. 5, November 1970)(11 votes)
- At8:24could you be more specific about what you mean with "some of these negative charges are going to need to leave". how does Na+ push away an anion ? (i suppose anion is what you mean by negative charge) Aren't an cation and anion atracting each other ?(7 votes)
- They do! However, with an influx of Na+, that part of the membrane will depolarize (i.e. become LESS negative). If you and your friends walk into a bus full of girls, even though you are all attracted to them, you can't physically occupy the same space as them, some of them will have to move so you can stand somewhere. As the ones standing right next to the bus door (negative charges next to the membrane) leave the area, other guys in the bus (who were attracted to them b/c of different charges) will move somewhere else b/c there is no dipole moment there (in the video, this is the positive charges moving into the intracellular fluid).(14 votes)
- At3:19does this mean that Na+ molecules travel in a straight line while in the cytoplasm of the cell?(2 votes)
- No he is not referring to that. He's trying to explain that with a larger diameter axon there is less possibility for the sodium ion to collide to with other structures with the cytosol. Hence, the sodium ion will be able to travel a greater distance in a larger axon and contribute more so to the action potential than an axon with a smaller diameter. Also, I think most molecules follow Brownian motion, move randomly/chaotically.(8 votes)
- Near the end he mentioned that the action potential generated at the nodes of Ranvier was necessary to keep the "momentum", what would happen if the space between nodes was too great (i.e. too much myelin) and the charge completely dissipated and couldn't make it past the next node? Is that just a misfire?(3 votes)
- the signal would dissipate and become weak, so that when the weak signal reach the next node it will not be strong enough to start an action potential.
Just like in the earlier videos were signals from the dendrites had to be strong enough to start the action potential.
So it would just be a misfire.(4 votes)
- At the nodes of Ranvier region of the axon, sodiun enters the axon via a Na channel changing the charge in the area of the axon at the Na channel to more positive. This movement of sodium ions across the Na channel depolarizes the axon. Depolarization is not dependent on the movement of anions on the inside of the axon "away from the membrane" is it? Aren"t the negative charges neutralized by the incoming Na ions, the Na ions on the exterior of the membrane do not need to "move away from the membrane" they already have by moving into the axon via the Na channel. Doesn't this describe the local (near the Na channel) events? For every Na that enters the axon via the Na channel one negative charge is neutralized decreasing the membrane potential (more positive), but the number of cations outside the axon and the number of anions inside the axon, while less, in number are still equal in number to each other, so... why would ions move away from the membrane?
At the proximal edge of an internodal region does the influx of Na through the Na channel more easily change the membrane potential because less Na has to enter the axon in order to neutralize the fewer anions in this area, explaining the speed with which the action potential moves in the internodal area?
Is this a reasonable explanation of the events in the distal node of Ranvier/proximal internodal area, or is my comment under the second question an analogy of what actually happens...
The Na ions move into the axon pushing the anions away from a discrete area of the interior of the membrane. This results in less anions in that area causing less of a dipole moment there. The sodium cations therefore move away from the area in response to the lesser dipole moment. Soooo the depolarization is a function not of charge neutralization but physical displacement of ions and a change in the dipole moment in discrete areas?(2 votes)
- Two quick questions
1. From what you've said, the most efficient way (time and energy wise), to pass a signal through a neuron, is to have the action potential initiated from a point as close to the axon terminal as possible (perhaps a connection directly to the end of a target cell's axon). Theoretically, what would the effect be, on an individual, if the majority of his neuron connections where to axons (thus reducing the distance needed to be travelled by action potentials)?
2. If an action potential is initiated, by neurotransmitters, some point further along the axon, is it possible for the action potential to propagate backward (toward the hillock)?(2 votes)
- 1. The action potential is initiated at the axon hillock or the trigger zone. This area is not necessarily near the terminal. The action potential is only propagated if the threshold at the axon hillock is reached.
2. Since (1.) is true, the action potential always goes from the axon hillock to the terminals or synapse. There is a refractory period that prevents the 'backward direction' of the action potential.
- At8:26why does the negative ions leave the inside of the membrane and mix with the rest of the ion in the cytoplasm?
Same with the positive ions on the outside.
Thank you in advance!(1 vote)
- Ions usually move by diffusion or by active transport. Here are some videos that might help:Start here:
- Why does a smaller tubule diameter increase "conduction speed" in blood flow, but decrease conduction speed in nerve impulses?(1 vote)
- Do you mean conduction speed in blood flow or the amount of pressure in a artery or vein as a result of decreasing diameter. This would increase pressure because pressure is defined as force per unit area. Decreasing the unit area would increase the force.(1 vote)
- If the neuron is myelinated from the start of axon till the end then will there be nerve impulse conduction? Because transmbrane proteins are absent throughout the length and the nodes of ranvier are absent? Will there be such a long jump?(1 vote)
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.