INDUCTION OF JUND MESSENGER-RNA AFTER TRANSIENT FOREBRAIN ISCHEMIA INTHE RAT - EFFECT OF HYPOTHERMIA

The expression of junD was studied in the rat hippocampus by in situ h ybridization after 15 min of normothermic (37 degrees C) and hypotherm ic (33 degrees C) transient forebrain ischemia. Ischemia was induced b y common carotid artery occlusion combined with hypotension leading to damage in the CA1 region of the hippocampus which was prevented by hy pothermia. junD mRNA was induced in the hippocampus within 2 h of repe rfusion and was strong in the dentate gyrus but weak in the CA3 and CA 1 subregions. Intraischemic hypothermia significantly augmented the ju nD induction in the dentate gyrus. During late reperfusion (between 12 and 36 h after ischemia) a transient increase in junD mRNA was seen i n the normothermic CA3 which was abolished in the hypothermic brains. In contrast, in the normothermic CA1 a continuous increase of junD was seen. This was significantly reduced by intraischemic hypothermia. We suggest that the early induction in junD expression in the dentate gy rus and in the hypothermic CA3 region is a protective reaction to the ischemic stress. The marked increase in resistant brain areas could be due to the preserved intracellular signaling pathways and a subsequen t maintenance of protein synthesis. The late continuous increase, uniq ue to the vulnerable normothermic CA1 region, suggests that junD parti cipates in a transcriptional process that may be important for delayed neuronal death in the hippocampus following transient forebrain ische mia.