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Delayed antagonism of calpain reduces excitotoxicity in cultured neurons.

Authors
Type
Published Article
Journal
Stroke; a journal of cerebral circulation
Publication Date
Volume
26
Issue
7
Identifiers
PMID: 7541574
Source
Medline
License
Unknown

Abstract

The activation of calpain is among several enzymatic processes that contribute to the toxicity of glutamate receptor stimulation, and blocking these postreceptor mechanisms can be effective in protecting neurons from excitotoxicity at delayed time points.

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