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Nitric oxide and S ‐nitrosylation: excitotoxic and cell signaling mechanism
Author(s) -
Nelson Eric J,
Connolly Jon,
McArthur Patrick
Publication year - 2003
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/s0248-4900(03)00004-2
Subject(s) - excitotoxicity , neuroprotection , nitric oxide , glutamate receptor , biology , nmda receptor , neuroscience , mediator , microbiology and biotechnology , signal transduction , oxidative stress , excitatory postsynaptic potential , receptor , pharmacology , biochemistry , endocrinology , inhibitory postsynaptic potential
This review focuses on the important physiological messenger, nitric oxide (NO), and its role in N ‐methyl‐D‐aspartate (NMDA) excitotoxicity. NO has been shown to be a key mediator of voltage‐gated Ca +2 transmembrane proteins. It remains unclear whether NO is implicated during hypoxia, or ischemic/reperfusion injuries as a neuroprotective or neurodegenerative factor. Excitotoxicity results from the excessive stimulation of excitatory glutamate receptors within the CNS. This review maintains that the feed‐forward pathway precipitated by oxidative stress is the discriminating factor in the neuroprotective or neurodegenerative actions of NO.