Literature DB >> 10571239

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

W K Kim1, Y B Choi, P V Rayudu, P Das, W Asaad, D R Arnelle, J S Stamler, S A Lipton.   

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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Year:  1999        PMID: 10571239     DOI: 10.1016/s0896-6273(00)80859-4

Source DB:  PubMed          Journal:  Neuron        ISSN: 0896-6273            Impact factor:   17.173


  46 in total

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10.  Nitric oxide-NGF mediated PPTA/SP, ADNP, and VIP expression in the peripheral nervous system.

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