Modulation of nitric oxide homeostasis in a mouse model of spinal cord injury

Tiziana Genovese, Emanuela Mazzon, Sofia Mariotto, Marta Menegazzi, Salvatore Cardali, Alfredo Conti, Hisanori Suzuki, Placido Bramanti, Salvatore Cuzzocrea

Research output: Contribution to journalArticlepeer-review


Object. A traumatic spinal cord injury (SCI) immediately induces primary damage, and this is followed by secondary damage characterized by a series of events among which is a progressive extension of cell death within the damaged tissue. In this study, the authors investigated the role of inducible nitric oxide synthase (iNOS) in an experimental model of SCI in mice. Methods. In wild-type (iNOS+/+) mice, SCI rapidly induced an inflammatory response as shown by nitrotyrosine formation, activation of the nuclear enzyme poly(adenosine diphosphate-ribose) polymerase (PARP), neutrophil infiltration, and spinal cord tissue histopathological changes, indicating the involvement of iNOS-derived massive amounts of NO in SCI. Conclusions. Genetic inhibition of iNOS, however, resulted in a significant reduction in secondary damage, and this therapeutic efficacy was associated with the prevention of an SCI-induced drop in neuronal and endothelial NOS activity.

Original languageEnglish
Pages (from-to)145-153
Number of pages9
JournalJournal of Neurosurgery: Spine
Issue number2
Publication statusPublished - Feb 2006


  • Inducible nitric oxide synthetase
  • Mouse
  • Oxidative stress
  • Poly(adenosine diphosphate-ribose)
  • Secondary injury
  • Spinal cord injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery
  • Neurology


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