Effects of hypoxia on ischemic delayd neuronal death

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1. Gerbils were exposed to 10% oxygen in a chamber for 3 weeks. The bilateral carotid arteries at the neck were occluded for 5 minutes under halothane anaesthesia, recirculated and fed in a normoxia. Animals were sacrificed before and 2,4, and 7 days after surgery. Immunohistochemical study was also done with antibodies against basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF). The neuronal death in the hippocampus was severer in the hypoxic group. Expression of both bFGF and VEGF was obvious in the cingulate cortex, corpus callosum and internal capsule before clipping in the hypoxic group, but not observed in the normoxic group before clipping. We observed the expression of both bFGF and VEGF widely in the brain at 2 and 4 days sfter recirculation in both groups. The expression in the hypoxic group was much more prominent than that in the normoxic group. These expressions were not observed at 7 days in both groups.2. Using a differential display technique, we examined the changes in expression of mRNAs in the hippocampus following 5-minute cerebral ischemia in normoxic Mongolian gerbils. Gerbils were divided into 3 groups (control, 6 hours, 2 days). mRNAs were classified into 3 patterns ; gradual disappearance, decrease and recovery, and new appearance. An mRNA species expressed in the hippocampus in the control group but which decreased at 6 hours after cerebral ischemia and disappeared at 2 days was subcloned and sequenced partly. This mRNA showed homology to neuronal pentraxin. In situ hybridization and Northern blot analyzes showed the same changes in expression as shown by the differential display technique. Neither Western blot nor immunohistochemical analyzes showed differences in neuronal pentraxin protein level among the 3 groups. This observation suggested that neuronal pentraxin plays an important role in delayd neuronal death.