期刊
TRENDS IN PHARMACOLOGICAL SCIENCES
卷 25, 期 11, 页码 584-591出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2004.09.001
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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.
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