Alcohol, nitric oxide, and neurotoxicity: is there a connection?--a review.
A hypothesis is presented to explain the influence of alcohol on glutamate generated excitotoxicity. Chronic alcohol exposure is reported to increase glutamate-N-methyl-D-aspartate (NMDA) receptors and calcium ion channel activity, resulting in the neurotoxicity and seizure activity associated with alcohol withdrawal in certain persons. Recent information indicates that nitric oxide is responsible for the neurotoxicity associated with excessive glutamate stimulation of NMDA receptors. Thus, it is hypothesized that nitric oxide is involved in producing the neurotoxicity and cell disturbances associated with chronic alcohol exposure.
Lancaster
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Division of Basic Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857.
D000818:Animals; D001921:Brain / Q000187:drug effects*; D001925:Brain Damage, Chronic / Q000139:chemically induced*; D015220:Calcium Channels / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D000431:Ethanol / Q000633:toxicity*; D006801:Humans; D009410:Nerve Degeneration / Q000187:drug effects; D009569:Nitric Oxide / Q000633:toxicity*; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects; D017981:Receptors, Neurotransmitter / Q000187:drug effects
D015220:Calcium Channels; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D009569:Nitric Oxide; D000431:Ethanol