Nitroxyl anion regulation of the NMDA receptor.

Published

Journal Article

Nitric oxide (NO) is an important regulator of NMDA channel function in the CNS. Recent findings suggest that nitroxyl anion (NO(-)) may also be generated by nitric oxide synthase, which catalyzes production of NO. Using recombinant NMDA receptors (NMDA-r) transfected into human embryonic kidney cells, our data demonstrate that the nitroxyl anion donor, Angeli's salt (AS; Na(2)N(2)O(3)) dramatically blocked glycine-independent desensitization in NMDA-r containing NR1-NR2A subunits. AS did not affect glycine-dependent desensitization, calcium dependent inactivation or glutamate affinity for the NMDA-r. This effect could be mimicked by treatment with DPTA, a metal chelator and was not evident under hypoxic conditions. In contrast, receptors containing the NR1-NR2B subunits demonstrated an approximate 25% reduction in whole cell currents in the presence of AS with no apparent change in desensitization. Our data suggest that the regulation of NMDA-r function by nitroxyl anion is distinctly different from NO and may result in different cellular outcomes compared with NO.

Full Text

Duke Authors

Cited Authors

  • Colton, CA; Gbadegesin, M; Wink, DA; Miranda, KM; Espey, MG; Vicini, S

Published Date

  • September 2001

Published In

Volume / Issue

  • 78 / 5

Start / End Page

  • 1126 - 1134

PubMed ID

  • 11553686

Pubmed Central ID

  • 11553686

International Standard Serial Number (ISSN)

  • 0022-3042

Language

  • eng

Conference Location

  • England