Ornithine decarboxylase knockdown exacerbates transient focal cerebral ischemia-induced neuronal damage in rat brain

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

Research output: Contribution to journalArticle

15 Scopus citations


Transient cerebral ischemia leads to increased expression of ornithine decarboxylase (ODC). Contradicting studies attributed neuroprotective and neurotoxic roles to ODC after ischemia. Using antisense oligonucleotides (ODNs), the current study evaluated the functional role of ODC in the process of neuronal damage after transient focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) in spontaneously hypertensive rats. Transient MCAO significantly increased the ODC immunoreactive protein levels and catalytic activity in the ipsilateral cortex, which were completely prevented by the infusion of antisense ODN specific for ODC. Transient MCAO in rats infused with ODC antisense ODN increased the infarct volume, motor deficits, and mortality compared with the sense or random ODN-infused controls. Results of the current study support a neuroprotective or recovery role, or both, for ODC after transient focal ischemia.

Original languageEnglish (US)
Pages (from-to)945-954
Number of pages10
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number8
StatePublished - Aug 20 2001



  • Antisense knockdown
  • Cerebral ischemia
  • Infarct
  • Middle cerebral artery occlusion
  • Neuronal damage
  • Ornithine decarboxylase

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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