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More MS news articles for November 2002

Neuroprotection of axons with phenytoin in experimental allergic encephalomyelitis

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12395089&dopt=Abstract

Neuroreport 2002 Oct 28;13(15):1909-12
Lo AC, Black JA, Waxman SG.

Voltage-gated sodium channels contribute to the development of axonal degeneration in white matter, and sodium channel blocking drugs are known to have a protective effect on acutely injured white matter axons.

To determine whether phenytoin has a protective effect on axons in a neuroinflammatory model, we studied the effect of phenytoin on axonal degeneration in the optic nerve in MOG-induced experimental allergic encephalomyelitis (EAE).

We report that, whereas approximately 50% of optic nerve axons are lost at 27-28 days in untreated EAE, only approximately 12% of the axons are lost if mice with MOG-induced EAE are treated with phenytoin.

These results demonstrate that it is possible to achieve substantial protection of white matter axons in EAE, a model neuroinflammatory/demyelination disease, with a sodium channel blocking agent.