What I mean to ask is that why should the nerve conduction jump in the first place in presence of myelin. It seems to be a conundrum as conduction needs a conduction and myelin is, in effect, an insulator. How does this property reconcile with the saltatory conduction?
Does this property have any role in neurodegeneration? It is just an additional thought that I think will be relevant.
Dear colleague
Please read this paper and it will help you understand the point.
Article Evidence for saltatory conduction in peripheral myelinated fibres
Thank you
‘Saltatory conduction’ is actually a nickname. Action potentials do not ‘jump’, nor do they even ‘travel’ along an axon, myelinated or not. The term action potential refers to a measurable fluctuation of the potential difference between an intracelular and an extracellular electrode, which arises as a consequence of ionic fluxes across plasma membrane channels. Each action potential is a local event generated at a very small patch of the membrane, where there is a high concentration of a particular type of sodium channel. The source of the rapid depolarization known as the action potential is actually the massive influx of sodium ions through such voltage-gated sodium channels. These channels are more or less evenly distributed along the plasma membrane of unmyelinated axons, but they are for the most part restricted to the Ranvier nodes in myelinated axons. The fact that individual action potentials in a normal myelinated axon are generated at succesive Ranvier nodes leads to the appearance of a saltatory phenomenon. In reality, however, each spike is a single event. What drives the conduction of action potentials along the axon are electrotonic currents between the segment of the axon where an action potential has just been generated, and the rest of the axon ahead of that region, along the longitudinal dimension of the fiber (forward intracellularly, backward extracellularly). Myelin helps focus such currents into each node of Ranvier not quite because of its electrical resistance, but mostly because of the low capacitance of the myelin stack, which drains very little current through the membrane and leaves most of those local currents to spread longitudinally and sink into the concentrated voltage-gated sodium channels at the next Ranvier node. Then and there, the current drives the opening of those channels, a brand new action potential is generated, and so on.
Dear Dr. Saleh,
I have already read the paper you have given the link to. It is not addressing my concern. It just is one of the earliest evidences of saltatory conduction in myelinated neurons. My question is different which has been, to some extent, addressed by Prof. Linden above.
If you have a better answer or any details that would be relevant, I will be thankful. But please read the description of y question before your paste a link in the answer.
Thanks
hello
regarding the last part of your question that is if myelin play a role in neurodegeneration
on the contrary, Schwann cell play important role in neuronal regeneration and nerve repair and this role makes the PNS nerve injury more likely to heal than CNS
I'm not sure saltatory is the best term to use for propagation along a myelinated axon. See https://hobbieroth.blogspot.com/2012/03/saltatory-conduction.html
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