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• W2071553665 startingPage "179" @default.
• W2071553665 abstract "Derangements in glutamate neurotransmission have been implicated in several neurodegenerative disorders including, stroke, epilepsy, Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS). Activation of the N-methyl-d-aspartate (NMDA) receptor subtype of glutamate receptors results in the influx of calcium which binds calmodulin and activates neuronal nitric oxide synthase (nNOS), to convent l-arginine to citrulline and nitric oxide (NO). NO has many roles in the central nervous system as a messenger molecule, however, when generated in excess NO can be neurotoxic. Excess NO is in part responsible for glutamate neurotoxicity in primary neuronal cell culture and in animal models of stroke. It is likely that most of the neurotoxic actions of NO are mediated by peroxynitrite (ONOO−), the reaction product from NO and superoxide anion. In pathologic conditions, peroxynitrite and oxygen free radicals can be generated in excess of a cell antioxidant capacity resulting in severe damage to cellular constitutents including proteins, DNA and lipids. The inherent biochemical and physiological characteristis of the brain, including high lipid concentrations and energy requirements, make it particularly susceptible to free radical and oxidant mediated insult. Increasing evidence indicates that many neurologic disorders may have components of free radical and oxidative stress induced injury." @default.
• W2071553665 created "2016-06-24" @default.
• W2071553665 creator A5021759485 @default.
• W2071553665 creator A5025568267 @default.
• W2071553665 date "1996-06-01" @default.
• W2071553665 modified "2023-10-18" @default.
• W2071553665 title "Nitric oxide neurotoxicity" @default.
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• W2071553665 doi "https://doi.org/10.1016/0891-0618(96)00148-2" @default.
• W2071553665 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8811421" @default.
• W2071553665 hasPublicationYear "1996" @default.
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