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Nitric Oxide Synthase Isoforms Undertake Unique Roles During Excitotoxicity
Author(s) -
Susana R. Parathath,
Iordanis Gravanis,
Stella E. Tsirka
Publication year - 2007
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.106.478826
Subject(s) - excitotoxicity , neurodegeneration , neuroprotection , endothelial nos , nitric oxide synthase , nitric oxide , glutamate receptor , neuroscience , medicine , pharmacology , microbiology and biotechnology , biology , enos , receptor , disease
Excitotoxicity is a component of many neurodegenerative diseases. The signaling events that lead from excitotoxic injury to neuronal death remain incompletely defined. Pharmacological approaches have shown that nitric oxide production is critical for the progression of neurodegeneration after the initiation of excitotoxicity by the glutamate analog kainate. Although nitric oxide additionally triggers blood-brain barrier (BBB) breakdown, the breakdown does not in itself inevitably lead to neuronal cell death, because neuroprotective pharmacological means can be used subsequently to prevent the neural death.

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