MORPHO-FUNCTIONAL CHANGES OF HIPPOCAMPAL CA1 AREA IN MONGOLIAN GERBILS AFTER ISCHEMIC POSTCONDITIONING



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Abstract

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).

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