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I am trying to understand why the myelin sheaths would make a difference in conduction

- I know that the axon is long so since L is proportional to resistance then the electrical current will dissipate in long distances
- If we add myelin sheaths the Area will increase so the resistance will decrease

(i'm using R= (rho*L)/A))

Now if we add myelin sheaths sodium and potassium channels will only be located where there is no myelin so at the nodes of ranvier but why does it have any effect at all ? If potassium and sodium channels are located all along the axon without myelin why can't the electrical signal increase again to avoid dissipation?

Not sure that my question makes sense but basically how does the myelin sheath help if we look at the physics of it?

Thanks!

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Segmental myelination of nerve axons is a neat trick that evolved to improve the spatial precision and speed of signal propagation within the nervous system. It obviously improves the spatial precision, especially over long signal pathways, by insulating axons from the effects of electrical interference (potentially confusing "cross-talk") from nearby neuronal activity, and this becomes more important for longer axons. It is less clear why myelination would increase signal conduction speed.

So ask yourself why there are nodes of Ranvier in these myelinated axons if the sole purpose of myelin is to increase signal spatial precision? Wouldn't it be best to have just one very long insulated axon to transmit signal along the entire nerve? The answer is no, and for physical reasons that have to do with passive electrotonic propagation within the axon. The myelin does effectively increase the length constant of the axon, which means that voltage dissipation is less than it would be for unmyelinated axons, but it's still present and the signal would die out and not make it to the end of the exon. It needs to be "boosted" to keep propagating, and this occurs at the nodes of Ranvier. At these sites there are ion channels that generate action potentials, and you can think of these as signal "booster" sites. Unmyelinated axons have ion channels distributed all along their length, because these are needed to frequently boost their dissipating signals. Why not just dispense with the myelin altogether? Well, it does take a bit of time for ion channels to open and generate the ion flux that makes the action potential and by increasing the length constant myelination allows the axons to "skip" this need for signal boosting to much fewer points along the axon signal path. When you calculate the amount of time it takes for action potential generation and propagation along axons with and without myelination in various configurations, you will find that the nervous system has evolved an ingenious way to both speed up and make more precise signal transmission.

BTW, I was taught a neat way to understand what all this means during my training. With your thumb and forefinger of one hand, flick a fingernail against the nail of a finger on the other hand. The first thing you will feel, almost immediately, is a sharp very localized pain in the struck fingernail. This will be followed a bit latter by a more throbbing somewhat less localized "deeper" pain. A major (but not the only) reason for these differences is that the nerves conducting the first pain sensation are myelinated and those responsible for the second sensation are not.
 
Segmental myelination of nerve axons is a neat trick that evolved to improve the spatial precision and speed of signal propagation within the nervous system. It obviously improves the spatial precision, especially over long signal pathways, by insulating axons from the effects of electrical interference (potentially confusing "cross-talk") from nearby neuronal activity, and this becomes more important for longer axons. It is less clear why myelination would increase signal conduction speed.

So ask yourself why there are nodes of Ranvier in these myelinated axons if the sole purpose of myelin is to increase signal spatial precision? Wouldn't it be best to have just one very long insulated axon to transmit signal along the entire nerve? The answer is no, and for physical reasons that have to do with passive electrotonic propagation within the axon. The myelin does effectively increase the length constant of the axon, which means that voltage dissipation is less than it would be for unmyelinated axons, but it's still present and the signal would die out and not make it to the end of the exon. It needs to be "boosted" to keep propagating, and this occurs at the nodes of Ranvier. At these sites there are ion channels that generate action potentials, and you can think of these as signal "booster" sites. Unmyelinated axons have ion channels distributed all along their length, because these are needed to frequently boost their dissipating signals. Why not just dispense with the myelin altogether? Well, it does take a bit of time for ion channels to open and generate the ion flux that makes the action potential and by increasing the length constant myelination allows the axons to "skip" this need for signal boosting to much fewer points along the axon signal path. When you calculate the amount of time it takes for action potential generation and propagation along axons with and without myelination in various configurations, you will find that the nervous system has evolved an ingenious way to both speed up and make more precise signal transmission.

BTW, I was taught a neat way to understand what all this means during my training. With your thumb and forefinger of one hand, flick a fingernail against the nail of a finger on the other hand. The first thing you will feel, almost immediately, is a sharp very localized pain in the struck fingernail. This will be followed a bit latter by a more throbbing somewhat less localized "deeper" pain. A major (but not the only) reason for these differences is that the nerves conducting the first pain sensation are myelinated and those responsible for the second sensation are not.

Thanks a lot for the detailed response.
What do you mean by "The myelin does effectively increase the length constant of the axon"?

And so, here is how I am understanding this correct me if I'm wrong.
- If we had no myelination every sodium channel would have to open which would take a lot of time and since resistance increases with length the current would slow down.
- If we had myelination along the entire axon then myelin is an insulator so it has high resistance and doesn't let the current leave across the membrane but since sodium channels won't be present and we still have the same issue with the length then the signal will also be dissipated.
- With the nodes of ranvier, we have the myelin sheaths that protect from current being loss outside the membrane but we also have the nodes of ranvier where we can "recharge" the signal which is propagating.

Thanks A LOT!
 
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