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 a...

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Bibliographic Details
Published inTrends in pharmacological sciences (Regular ed.) Vol. 25; no. 11; pp. 584 - 591
Main Authors Waxman, Stephen G., Craner, Matthew J., Black, Joel A.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.11.2004
Subjects
Animals
Axons - metabolism
Axons - pathology
Disease Models, Animal
Humans
Multiple Sclerosis - metabolism
Multiple Sclerosis - pathology
Protein Isoforms
Sodium Channels - classification
Sodium Channels - metabolism
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Summary: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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-2
ISSN:0165-6147
1873-3735
DOI:10.1016/j.tips.2004.09.001