Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and l-[3H]nitroarginine binding

Vemuganti L. Raghavendra Rao, Aclan Dogan, Kellie K. Bowen, Robert J. Dempsey

Research output: Contribution to journalArticle

43 Scopus citations


Overstimulation of N-methyl-o-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The present study examined the mRNA and protein levels of nNOS in the ipsilateral and contralateral cortex of rats as a function of time (5 minutes to 1 week) after controlled cortical impact (CCI) brain injury. Sham-operated rats served as controls. TBI resulted in a significant increase in the levels of nNOS mRNA (1.5- to 2.8-fold, p < .05) between 2 and 4 hours after the injury. There was also a significant increase in the levels of nNOS protein (by 55% to 90%, p < .05) and binding densities of the nNOS-specific ligand L- [3H]nitroarginine (L-[3H]NOARG) (by 35% to 59%, p < .05) between 2 and 12 hours after the injury. Increased nNOS expression and function may contribute to the concomitant excitotoxic neuronal death after TBI.

Original languageEnglish (US)
Pages (from-to)865-877
Number of pages13
JournalJournal of neurotrauma
Issue number10
StatePublished - Oct 1 1999
Externally publishedYes



  • L-nitroarginine
  • Neuronal nitric oxide synthase
  • Nitric oxide
  • RT- PCR
  • Traumatic brain injury
  • Western blotting
  • mRNA

ASJC Scopus subject areas

  • Clinical Neurology

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