Hypothermic, but not normothermic, ischemia causes a drastic increase in cyclooxygenase-2 immunoreactive granule cells in rat dentate gyrus after 4 hours of ischemic reperfusion.

We investigated cyclooxygenase-2 (Cox-2) immunoreactive cells in the hippocampus and dentate gyrus of Sprague-Dawley rats at 4 h after the induction of normothermic and hypothermic ischemia and reperfusion. Under the normothermic condition, Cox-2 immunoreactive cells showed more intense staining and clearer proximal dendrite configurations as compared with the control animals, whereas the numbers of immunoreactive cells in the hippocampus and dentate gyrus were not remarkably increased. In contrast to the normothermic condition, long-term (pre- and intra-ischemic) and short-term (exclusively intra-ischemic) hypothermic conditions caused a drastic increase in immunoreactive cells in the dentate gyrus. Nearly all granule cells were immuno-positive for Cox-2, whereas the CA3 and hilus sectors showed no remarkable increase in immunoreactive cell numbers. In sham-operated animals exposed to long-term hypothermia - but not ischemia, Cox-2 staining profiles were similar to those in the control animals. These results suggest that, for a drastic increase in Cox-2 immunoreactive granule cells to occur within a short time period (4 h), at a minimum, both hypothermia and ischemia, are required. Considering the neuroprotective roles of the hypothermia, a rapid increase in Cox-2 in the dentate gyrus might be associated with this temperature-sensitive phenomenon.