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Attenuation of NMDA receptor activity and neurotoxicity by nitroxyl anion, NO-
- Authors
- Kim W.-K.; Choi Y.-B.; Rayudu P.V.; Das P.; Asaad W.; Arnelle D.R.; Stamler J.S.; Lipton S.A.
- Issue Date
- 1999
- Publisher
- Cell Press
- Citation
- Neuron, v.24, no.2, pp 461 - 469
- Pages
- 9
- Indexed
- SCOPUS
- Journal Title
- Neuron
- Volume
- 24
- Number
- 2
- Start Page
- 461
- End Page
- 469
- ISSN
- 0896-6273
1097-4199
- 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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Collections - 1. Basic Science > Department of Neuroscience > 1. Journal Articles
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Related Researcher
- Kim, Won Ki
- College of Medicine (Department of Neural Sciences)