Neuron
Volume 24, Issue 2, October 1999, Pages 461-469
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Article
Attenuation of NMDA Receptor Activity and Neurotoxicity by Nitroxyl Anion, NO

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Abstract

Recent evidence indicates that the NO-related species, nitroxyl anion (NO), is produced in physiological systems by several redox metal–containing proteins, including hemoglobin, nitric oxide synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identified in brain. However, the chemical biology of NO remains largely unknown. Here, we show that NO—unlike NO·, but reminiscent of NO+ transfer (or S-nitrosylation)—reacts mainly with Cys-399 in the NR2A subunit of the N-methyl-D-aspartate (NMDA) receptor to curtail excessive Ca2+ influx and thus provide neuroprotection from excitotoxic insults. This effect of NO closely resembles that of NOS, which also downregulates NMDA receptor activity under similar conditions in culture.

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