Attenuation of NMDA receptor activity and neurotoxicity by nitroxyl anion, NO-

Won Ki Kim, Yun Beom Choi, Posina V. Rayudu, Prajnan Das, Wael Asaad, Derrick R. Arnelle, Jonathan S. Stamler, Stuart A. Lipton

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179 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)461-469
Number of pages9
JournalNeuron
Volume24
Issue number2
DOIs
Publication statusPublished - 1999 Oct
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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    Kim, W. K., Choi, Y. B., Rayudu, P. V., Das, P., Asaad, W., Arnelle, D. R., Stamler, J. S., & Lipton, S. A. (1999). Attenuation of NMDA receptor activity and neurotoxicity by nitroxyl anion, NO-. Neuron, 24(2), 461-469. https://doi.org/10.1016/S0896-6273(00)80859-4