Neonatal mice lacking neuronal nitric oxide synthase are less vulnerable to hypoxic-ischemic injury

Donna M. Ferriero, David M. Holtzman, Stephen Matthew Black, R. Ann Sheldon

Research output: Contribution to journalArticle

164 Citations (Scopus)

Abstract

We hypothesized that elimination of neuronal nitric oxide synthase (nNOS) by targeted disruption of the nNOS gene would result in amelioration of damage seen after hypoxia-ischemia in the developing brain since nitric oxide (NO) has been implicated in glutamate-mediated neurotoxicity after ischemia. Both wildtype and nNOS-deficient pups were subjected to focal ischemia followed by 1.5 h of hypoxia at Postnatal Day 7. Seven days later, brains of surviving animals were analyzed for damage. The nNOS-deficient pups (n = 17) had less histopathologic evidence of injury in both the hippocampus (P = 0.008) and the cortex (P = 0.0008) than the wildtype (n = 30) mice. When injured, the nNOS-deficient mice had damage that was limited to the hippocampus. These results support a role for neuronally produced NO in injury after perinatal hypoxia-ischemia.

Original languageEnglish (US)
Pages (from-to)64-71
Number of pages8
JournalNeurobiology of Disease
Volume3
Issue number1
DOIs
StatePublished - Jan 1 1996

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Nitric Oxide Synthase Type I
Ischemia
Wounds and Injuries
Hippocampus
Nitric Oxide
Brain
Glutamic Acid
Genes
Hypoxia

ASJC Scopus subject areas

  • Neurology

Cite this

Neonatal mice lacking neuronal nitric oxide synthase are less vulnerable to hypoxic-ischemic injury. / Ferriero, Donna M.; Holtzman, David M.; Black, Stephen Matthew; Sheldon, R. Ann.

In: Neurobiology of Disease, Vol. 3, No. 1, 01.01.1996, p. 64-71.

Research output: Contribution to journalArticle

Ferriero, Donna M. ; Holtzman, David M. ; Black, Stephen Matthew ; Sheldon, R. Ann. / Neonatal mice lacking neuronal nitric oxide synthase are less vulnerable to hypoxic-ischemic injury. In: Neurobiology of Disease. 1996 ; Vol. 3, No. 1. pp. 64-71.
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