NEUR 310 Lecture Notes - Lecture 8: Myelin Basic Protein, Experimental Autoimmune Encephalomyelitis, Squid Giant Axon

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ivorykangaroo940

5 Feb 2017

School

McGill University

Department

Neurology and Neurosurgery

Course

NEUR 310

Professor

Jean- Francois Cloutier

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Document Summary

Axon conduction speed - speed of conduction of action potential. Squid giant axon: largest known axon, very fast conduction: but, diameter of a pencil lead - too much space needed. Insulate, add in active booster stations: saltatory conduction: action potential jumps from one booster station to the next, 10 x faster than conduction in an unmyelinated axon of the same diameter. Invertebrates, which generally lack myelin, achieve high rates of impulse conduction simply by increasing the radius of their axons. Myelinated and unmyelinated axons: unmyelinated neurons in invertebrates. In humans, most of our neurons are myelinated: motor neurons can be a meter long, sensory neurons are bipolar, and are also highly myelinated, non-myelinated neurons are c-fibres (pain sensory neurons) In some sense, the cns is more efficient. The membrane of the glial cell wraps around the axon inwardly: the membrane displaces the membrane that was already in contact with the axon, this makes the nucleus stay stationary.

Related Questions

How does spacing apart sodium and potassium channels allow theaction potential to travel faster down the axon? This is the reasonalways cited for saltatory conduction and myelination, but mymental model of conduction tells me that the density of ion gatesalong the axon should not affect the speed of the AP.

To illustrate, consider a myelinated axon. A wave of Na+ fromaction potential site 1, a node of Ranvier, rushes into and quicklydiffuses down the axon. (It travels in both directions, butbackwards is still in the refractory period.) It diffuses throughthe myelinated region, its concentration always diminishing. Beforeit 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 halfwaybetween node 1 and 2, called node 1.5. The wave of Na+, on its wayto node 2, happens to trigger an action potential at node 1.5, fromwhich a wave of Na+ pours in and either boosts the original wave orreplaces it by taking its momentum. Now the reinforced waveproceeds to node 2 and triggers it just as soon as, perhaps evensooner than, if node 1.5 had not existed. Repeatedly insert nodesat higher densities until the situation is simply lack ofmyelination, and we conclude that unmyelinated axons can transmitan action-potential-triggering wave of Na+ as fast as or fasterthan a myelinated one.

In short, my point of confusion is this: I cannot seehow a higher density of gated channels can possibly slow down thewavefront of Na+ that triggers action potentials. Ifanything, the additional influxes of Na+ should speed up theall-important wavefront, assuming that new waves really "eitherboost the original wave or replace it by taking its momentum", andalso assuming that the wavefront of Na+ is really all-important forsignal transmission, and also assuming that the mere presence of(voltage?) gated ion channels in the membrane does notsignificantly retard the wavefront.

But the usual explanation for why saltatory conduction is fasterthan continuous conduction (a fact I hope is empirically andunambiguously established) relies on the putativeslowing effect of ion channels on the signal fore. Please explainthis effect in more detail, if it is not amisconception.

NEUR 310 Lecture Notes - Lecture 8: Myelin Basic Protein, Experimental Autoimmune Encephalomyelitis, Squid Giant Axon

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