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

Transient cerebral ischemia leads to increased expression of ornithine deca rboxylase (ODC). Contradicting studies attributed neuroprotective and neuro toxic roles to ODC after ischemia. Using antisense oligonucleotides (ODNs), the current study evaluated the functional role of ODC in the process of n euronal damage after transient focal cerebral ischemia induced by middle ce rebral artery occlusion (MCAO) in spontaneously hypertensive rats. Transien t MCAO significantly increased the ODC immunoreactive protein levels and ca talytic activity in the ipsilateral cortex. which were completely pre-vente d by the infusion of antisense ODN specific for ODC. Transient MCAO in rats infused with ODC antisense ODN increased the infarct volume, motor deficit s, and mortality compared with the sense or random ODN-infused controls. Re sults of the current study support a neuroprotective or recovery role, or b oth, for ODC after transient focal ischemia.