Abstract
Age-related decreases in the conduction velocity (CV) of action potentials along myelinated axons have been linked to morphological changes in the myelin sheath. In particular, evidence suggests the presence of segmental demyelination and remyelination of axons. In remyelinated segments, the distance between adjacent nodes of Ranvier is typically shorter, and myelin sheaths are thinner. Both experimental and computational evidence indicates that shortened internodes slows CV. In this computational study, we determine the impact of progressive segmental demyelination and remyelination, modeled by shorter internodes with thinner myelin sheaths interspersed with normal ones, upon the CV. We find that CV progressively decreases as the number of remyelinated segments increases, but this decrease is greater than one would expect from an estimate of the CV based merely upon the number of short and long internodes. We trace the additional suppression of the CV to transitions between long and short internodes. Our study presents an important consideration for the precise modeling of neural circuits with remyelinated neurons.
Highlights
Action potentials (AP) are electrical signals propagated distally along the axon, prompted by an influx of current into the cell, and at synapses they result in the timely release of neurotransmitters necessary for neural communication
With the tight junctions (TJs) model we examine separately the impact that remyelinated segments with thinner myelin sheaths have on conduction velocity
We were able to quantitatively assess the impact of progressive segmental demyelination and remyelination, simulated by shorter internodes with thinner myelin sheaths interspersed with normal internodes, on the conduction velocity of action potentials
Summary
Action potentials (AP) are electrical signals propagated distally along the axon, prompted by an influx of current into the cell, and at synapses they result in the timely release of neurotransmitters necessary for neural communication. The timing of these signals depends, in part, on the conduction velocity (CV) of the AP along the axon. When an influx of charge in an otherwise quiescent axon results in a transthreshold depolarization, an AP is generated This phenomenon can be effectively modeled via a linear core-conductor model with membrane dynamics described by the Hodgkin-Huxley equations [1]. Conduction velocities roughly scale as d 1⁄2mmÀ 1 m/s where d is the diameter of the axon, so for, say, a 500 μm diameter squid giant axon, the CV is roughly 22 m/s, consistent with experimental measurements [1, 2]
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