Demyelinated axons show an increased number of sodium channels distributed along previously internodal segments, demonstrating plasticity that may aid in conduction recovery.
May support conduction recovery via sodium channel plasticity in demyelinated axons; leaves open translation to human neuropathies.
Voltage-gated sodium channels are largely localized to the nodes of Ranvier in myelinated axons, providing a physiological basis for saltatory conduction. What happens to these channels in demyelinated axons is not known with certainty. Experimentally demyelinated axons were examined by using a well-characterized, polyclonal antibody directed against sodium channels. Immunocytochemical and radioimmunoassay data were consistent with the distribution of an increased number of sodium channels along segments of previously internodal axon. These findings affirm the plasticity of sodium channels in demyelinated axolemma and may be relevant to understanding how axons recover conduction after demyelination.
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England et al. (1990) studied this question.