Serine racemase deletion protects against cerebral ischemia and excitotoxicity

Asif K. Mustafa, Abdullah S. Ahmad, Emil Zeynalov, Sadia K. Gazi, Gautam Sikka, Jeffrey T. Ehmsen, Roxanne K. Barrow, Joseph T. Coyle, Solomon H. Snyder, Sylvain Doré

Research output: Contribution to journalArticle

Abstract

D-Serine, formed from L-serine by serine racemase (SR), is a physilologic coagonist at NMDA receptors. Using mice with targeted deletion of SR, we demonstrate a role for D-serine in NMDA receptor-mediated neurotoxicity and stroke. Brain cultures of SR-deleted mice display markedly diminished nitric oxide (NO) formation and neurotoxicity. In intact SR knock-out mice, NO formation and nitrosylation of NO targets are substantially reduced. Infarct volume following middle cerebral artery occlusion is dramatically diminished in several regions of the brains of SR mutant mice despite evidence of increased NMDA receptor number and sensitivity.

Original languageEnglish (US)
Pages (from-to)1413-1416
Number of pages4
JournalJournal of Neuroscience
Volume30
Issue number4
DOIs
StatePublished - Jan 27 2010

ASJC Scopus subject areas

  • Neuroscience(all)

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  • Cite this

    Mustafa, A. K., Ahmad, A. S., Zeynalov, E., Gazi, S. K., Sikka, G., Ehmsen, J. T., Barrow, R. K., Coyle, J. T., Snyder, S. H., & Doré, S. (2010). Serine racemase deletion protects against cerebral ischemia and excitotoxicity. Journal of Neuroscience, 30(4), 1413-1416. https://doi.org/10.1523/JNEUROSCI.4297-09.2010