title: Nitric oxide and S-nitrosylation: excitotoxic and cell signaling mechanism.
abstract: 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.
authors.affiliation: Husson Science Research Institute, One College Circle, Bangor, ME 04401, USA.
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Nelson
authors.forename: Jon
authors.initials: J
authors.lastname: Connolly
authors.forename: Patrick
authors.initials: P
authors.lastname: McArthur
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002490:Central Nervous System / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate; D009569:Nitric Oxide