title: Na+ channel expression along axons in multiple sclerosis and its models.
abstract: 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.
authors.affiliation: Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, CT 06510, USA. stephen.waxman@yale.edu
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Waxman
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Craner
authors.forename: Joel A
authors.initials: JA
authors.lastname: Black
mesh_terms: 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*
chemical_list: D020033:Protein Isoforms; D015222:Sodium Channels