期刊
JOURNAL OF THE NEUROLOGICAL SCIENCES
卷 233, 期 1-2, 页码 27-35出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2005.03.003
关键词
sodium channel; experimental autoimmune encephalomyelitis (EAE); nitric oxide; demyelination; hypoxia; energy depletion
资金
- Multiple Sclerosis Society [592] Funding Source: Medline
Axonal degeneration is a major cause of permanent neurological deficit in multiple sclerosis (MS). The mechanisms responsible for the degeneration remain unclear, but evidence suggests that a failure to maintain axonal sodium ion homeostasis may be a key step that underlies at least some of the degeneration. Sodium ions can accumulate within axons due to a series of events, including impulse activity and exposure to inflammatory factors such as nitric oxide. Recent findings have demonstrated that partial blockade of sodium channels can protect axons from nitric oxide-mediated degeneration in vitro, and from the effects of neuroinflammatory disease in vivo. This review describes some of the reasons why sodium ions might be expected to accumulate within axons in MS, and recent observations suggesting that it is possible to protect axons from degeneration in neuroinflammatory disease by partial sodium channel blockade. (c) 2005 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据