Na+ channel expression along axons in multiple sclerosis and its models.
Following the loss of myelin from axons in multiple sclerosis, some axons recover the ability to conduct impulses despite the absence of an insulating sheath, providing a basis for remission of clinical deficits. By contrast, other axons degenerate and contribute to non-remitting clinical deficits and, thus, disability. Investigations using laboratory models of multiple sclerosis indicate that altered expression of two distinct isoforms of Na+ channels underlies these two processes, and the study of human tissue reveals similar changes in multiple sclerosis.
Waxman
Stephen G
SG
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, CT 06510, USA. stephen.waxman@yale.edu
Craner
Matthew J
MJ
Black
Joel A
JA
D000818:Animals; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D006801:Humans; D009103:Multiple Sclerosis / Q000378:metabolism* / Q000473:pathology; D020033:Protein Isoforms; D015222:Sodium Channels / Q000145:classification / Q000378:metabolism*
D020033:Protein Isoforms; D015222:Sodium Channels