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How does spacing apart sodium and potassium channels allow the action potential to travel faster down the axon? This is the reason always cited for saltatory conduction and myelination, but my mental model of conduction tells me that the density of ion gates along the axon should not affect the speed of the AP.

To illustrate, consider a myelinated axon. A wave of Na+ from action potential site 1, a node of Ranvier, rushes into and quickly diffuses down the axon. (It travels in both directions, but backwards is still in the refractory period.) It diffuses through the myelinated region, its concentration always diminishing. Before it attenuates too much, however, it happens upon node of Ranvier 2, where it triggers another action potential. A new wave of Na+ rushes in and the cycle repeats. This should be plain so far.

Now imagine that there is actually a node of Ranvier halfway between node 1 and 2, called node 1.5. The wave of Na+, on its way to node 2, happens to trigger an action potential at node 1.5, from which a wave of Na+ pours in and either boosts the original wave or replaces it by taking its momentum. Now the reinforced wave proceeds to node 2 and triggers it just as soon as, perhaps even sooner than, if node 1.5 had not existed. Repeatedly insert nodes at higher densities until the situation is simply lack of myelination, and we conclude that unmyelinated axons can transmit an action-potential-triggering wave of Na+ as fast as or faster than a myelinated one.

In short, my point of confusion is this: I cannot see how a higher density of gated channels can possibly slow down the wavefront of Na+ that triggers action potentials. If anything, the additional influxes of Na+ should speed up the all-important wavefront, assuming that new waves really "either boost the original wave or replace it by taking its momentum", and also assuming that the wavefront of Na+ is really all-important for signal transmission, and also assuming that the mere presence of (voltage?) gated ion channels in the membrane does not significantly retard the wavefront.

But the usual explanation for why saltatory conduction is faster than continuous conduction (a fact I hope is empirically and unambiguously established) relies on the putative slowing effect of ion channels on the signal fore. Please explain this effect in more detail, if it is not a misconception.

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This is similar to, but I think slightly different than… – kmm May 9 '13 at 19:35
@kmm Actually, my question is in some sense the polar opposite of that question. That one asks why the whole axon is not completely covered in myelin, whereas mine asks why myelin is useful at all. I can understand that without regularly replenishing the Na+ inside the axon, the signal attenuates. Its wavefront is not a 'block'; like the Romans (pardon the analogy), it diffuses its previous territory as well as advancing its border, weakening itself. – user7924 May 11 '13 at 18:07
up vote 10 down vote accepted

There are two factors that need to be taken into account here:

1. Myelination decreases membrance capacitance.

The rate at which sodium influx through a node can depolarize the axon at the next node is related to both the current and capacitance across the membrane (in addition to a few other factors). So while adding a new node to the axon would indeed increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes. So it doesn't help to move the nodes closer together. What if instead we increase the distance between nodes? In that case, the trade-off is reversed and conduction velocity is again decreased. So there is some optimal internodal distance at which conduction velocity is maximized, and it turns out most axons happen to have just that geometry. [See: Waxman, SG. 1980]

2. Action potentials are metabolically expensive.

The brain uses a lot of energy (about 20% of the body's metabolism at rest)! Maintaining the proper balance of ions inside the neuron is the major reason for this energy usage. Every action potential incurs metabolic cost and if we double the number of nodes along an axon, we (nearly) double the metabolic cost of propagating spikes down that axon. So although conduction velocity appears to be the primary determinant in the choice of internodal distance, it is important to remember that it is not the only factor the organism must take into account.

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Hi Luke! Thanks for the answer. StackExchange notified me about it only a couple of days ago, which is why I've taken a week to respond. I would like to add another important factor, which I had overlooked when I first posted: ion leakage (specifically, outgoing ion pumps). Myelination prevents leakage, which may slow down the wavefront IF we assume that an attenuated (less concentrated) wave travels slower down the axon. – user7924 Jun 24 '13 at 8:15
Certainly minimizing membrane conductance is another potential benefit of myelination. To maximize conduction velocity, we would ideally want the inter-nodal membrane to have very high resistance. I did not include that as part of the answer because the cell could (and in some cases does) achieve the same effect by simply localizing channels to the nodes. This could be done without myelin at all, so I'm not sure it should be considered one of the primary actions of myelin. – Luke Jun 24 '13 at 20:23
Wow! It is fascinating that the cell can localize channels to small points along the axon without myelin. Thanks a BUNDLE for taking the time to post. Although I give this answer the check mark, I certainly hope others are not discouraged from contributing their knowledge. – user7924 Jun 25 '13 at 2:45
I'd just like to add that, if your information is accurate, this discussion should be pretty interesting, since usually people seem to take it for granted that myelination simply allows the action potential to somehow "hop" from node to node, and therefore the signal is faster. That may be a useful abstraction somewhere, somewhen, but it has no physical meaning, I think. – user7924 Jun 25 '13 at 2:56
Regarding 1. You write: "... while adding a new node to the axon would indeed increase its ability to generate sodium current, it would also increase the capacitance ...". Why or how would it increase capacitance? Regarding 2. How does that (help to) answer the question at all? – Arta Nov 21 '15 at 2:06

While Luke's answer is perfectly correct, the answer can be given in a more intuitive manner.

First, the main point is that it is increased positive voltage (inside the axon) that opens the sodium ion channels to propagate the action potential. The question is: how fast can this voltage get to the sodium channels?

In an unmyelinated axon, the movement of voltage across the membrane is due to ion flux (i.e the flow of ions through the channels, the current), and this movement is limited by the time it takes for the sodium ions to diffuse into the axon.

On the other hand, in a myelinated axon, the first bolus of sodium enters at the axon hillock. Because the capacitance is low, this means that the voltage can propagate down the axon, not by ion diffusion, but as an electrical field. The electrical field carries the voltage force much much faster than ion diffusion. Therefore, when the ions first enter, the voltage force moves, basically at the speed of light to the next node, where the voltage force opens the sodium ion channels there.

So, by allowing the voltage to be carried by the electrical field, the effect is that the distance between the nodes is effectively eliminated. Myelinated axons conduct faster because they are >>effectively<< much shorter than unmyelinated axons.

Finally, the optimized distance between nodes mentioned by Luke is exactly that distance in a given type of neuron's axon where the voltage force decays to the bare minimum needed to activate the sodium ion channels at the next node.

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Hello Don! Again, StackExchange emails are sluggish.... That's a really dam good explanation, and if it had been given early I might have checkmarked it. I like how it truly explains 'hopping'. However, my understanding of capacitance is not as good as it should be, so I cannot totally grasp the mechanism here. Therefore I am a little skeptical. Could you point me to a resource confirming and developing your answer, so I can study it more closely? – user7924 Sep 28 '13 at 0:17
What stops the voltage from propagating down the axon as an electrical field in an unmyelinated axon? – Arta Nov 21 '15 at 2:24

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