[Mitochondrial redox change in gerbil hippocampus before and after transient ischemia].

To investigate the basis of neuronal vulnerability we studied mitochondrial redox changes in gerbil hippocampus before and after 5 minutes forebrain ischemia. The brain was frozen by in situ funnel freezing method, and grinned off coronally until exposure of hippocampus. Relative value of regional redox ratio (NAD+/NADH) was obtained from fluorescence signals of intrinsic fluorochromes, i.e., NADH (PN) and flavoproteins (Fp), using a high resolution fluorometer. We calculated a modified redox ratio MRR = FP/(Fp + PN). Each point is displayed in gray scales ranged 16 degrees corresponding to the MRR value of the point; black represents a low MRR value (reduced) and white represents a high value (oxidized). Pyramidal cell layers and the granule cell layers were seen as linear areas of high MRR. The stratum radiatum and stratum orience of the CA 1 subfield showed low MRR compared with other hippocampal regions. During ischemic period, MRR in all subfield of hippocampus had decreased but the decrease was more severe in CA 1 region than in another. Just after recirculation, MRR decreased transiently in dentate and CA 3 areas but was fully recovered in all hippocampal areas with the exception of CA 1 region, where the MRR decreased again 12 hours after recirculation. These results suggest that CA 1 area suffers more pronounced hyoxic condition (state V) than other less vulnerable regions during 5 minutes ischemia. The irreversible reduction of MRR in CA 1 area may result from continuing mitochondrial dysfunction, and this may cause lasting energy shortage in CA 1 neurons that eventually results in slowly progressive cell death.