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We analyzed changes in activity of SDH, one of the most important enzymes of the Krebs cycle, in the cytoplasm of hippocampal and cortical neurons of Mongolian gerbils (Meriones unguiculatus) at the early and delayed reperfusion period after global brain ischemia. The data indicate that SDH activity in pyramidal neurons of various hippocampal areas and in neurons of II, III and V layers of cerebral cortex after 7-min forebrain ischemia depends on both the localization of these neurons and duration of the postischemic reperfusion. SDH activity in neurons significantly increased on days 2 and 7 after reperfusion.

The aim of this study was to determine the effect of ischemic postconditioning (IP) on the viability of neurons in various hippocampal areas as well as on cytoplasmic activity of succinatedehydrogenase (SDH) in these cells in 30 male Mongolian gerbils (Meriones unguiculatus). Ischemic brain injury was induced by bilateral common carotid artery occlusion for 7 min. IP protocol comprised 3 cycles of 15 s of reperfusion/15 s of ischemia. After reperfusion for 48 h, the morphometric analysis was conducted, and SDH cytoplasmic activity was assessed using quantitative histochemistry in the pyramidal neurons of the hippocampal areas CA1, CA2, CA3, CA4. The experiment has demonstrated that 7-minute-long ischemia resulted in a significant decrease in the number of viable neurons in CA1 area (up to 24%) and in the CA3 (to 56%) of the hippocampus; besides, it lead to the elevation of SDH activity in the cytoplasm of the neurons in all the hippocampal areas as compared to that in sham-operated animals. The application of IP significantly increased the number of viable neurons in CA1 (up to 52.9%, P<0,01) and in CA3 areas of the hippocampus(up to 88%, P<0,05), and it was accompanied by reduction of SDH activity in surviving neurons in all the hippocampal areas.

The aim of this study was to determine the effect of ischemic postconditioning on hippocampal CA1 neuronal survival and cytoplasmic activity of lactate dehydrogenase (LDH) in the gerbil model of cerebral ischemia-reperfusion injury. Ischemia was induced by bilateral common carotid artery occlusion (for 7 min) in male Mongolian gerbils (Meriones unguiculatus). Ischemic postconditioning protocol comprised 3 cycles of 15 s reperfusion/15 s ischemia. After 48 h of reperfusion, CA1 neuronal death was detected by Nissl staining and the cytoplasmic LDH was demonstrated histochemically in CA1 area of the hippocampus with a quantitative cytophotometric assessment of the enzyme activity. The results have shown that 7 min ischemia resulted in a significant decrease in the number of viable neurons (up to 24%) in the CA1 area of hippocampus; in addition, it reduced the activity of LDH in these neurons (from 0.260 +/- 0.009 to 0.190 +/- 0.006 relative units). The application of ischemic postconditioning significantly increased the number of viable neurons (up to 52.9%, P < 0.01) in the CA1 area of hippocampus, and it was accompanied by an increase in the activity of LDH (0.240 +/- 0.008 relative units, P < 0.001).