Nitroxyl anion regulation of the NMDA receptor

C. A. Colton, M. Gbadegesin, D. A. Wink, K. M. Miranda, M. G. Espey, S. Vicini

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


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; Na2N2O3) 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.

Original languageEnglish (US)
Pages (from-to)1126-1134
Number of pages9
JournalJournal of neurochemistry
Issue number5
StatePublished - 2001


  • Angeli's salt
  • Glycine independent desensitization
  • Hypoxia
  • N-methyl-D-aspartate
  • Nitroxyl anion

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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