Abstract
The efficient propagation of action potentials along nervous fibers is necessary for animals to interact with the environment with timeliness and precision. Myelination of axons is an essential step to ensure fast action potential propagation by saltatory conduction, a process that requires highly concentrated voltage-gated sodium channels at the nodes of Ranvier. Recent studies suggest that the clustering of sodium channels can influence axonal impulse conduction in both myelinated and unmyelinated fibers, which could have major implications in disease, particularly demyelinating pathology. This comprehensive review summarizes the mechanisms governing the clustering of sodium channels at the peripheral and central nervous system nodes and the specific roles of their clustering in influencing action potential conduction. We further highlight the classical biophysical parameters implicated in conduction timing, followed by a detailed discussion on how sodium channel clustering along unmyelinated axons can impact axonal impulse conduction in both physiological and pathological contexts.
Highlights
Electrical axonal propagation of the action potential (AP) leads to chemical neurotransmission through synapses, which drive important nervous system functions such as motor output, control of visceral organs, encoding of sensory stimuli, and higher order cognitive processing
Synaptic input received by the neurons is integrated in the somatodendritic region [1] and the initiation of the AP occurs at a region called the axon initial segment (AIS) [2]
The AIS is enriched in voltage-gated ion channels, voltage-gated sodium channels (Nav) that permit the entry of depolarizing current in the form of Na? ions [2, 3]
Summary
Mechanisms of sodium channel clustering and its influence on axonal impulse conduction Sean A. This article is published with open access at Springerlink.com
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