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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Kim, WK; Choi, YB; Rayudu, PV; Das, P; Asaad, W; Arnelle, DR; Stamler, JS; Lipton, SA

Published Date

  • October 1999

Published In

Volume / Issue

  • 24 / 2

Start / End Page

  • 461 - 469

PubMed ID

  • 10571239

Pubmed Central ID

  • 10571239

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/s0896-6273(00)80859-4


  • eng

Conference Location

  • United States