The effects of cerebral hypoxia on intracellular Ca^<2+> concentration

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Intracellular calcium plays a crucial role on cell damage in the case of hypoxia. These experiments were perfomed in order to investigate following objects.1) Measurement of intracellular Cs^<2+> concentration using calcium fluorescent dye, Quin2, and the effects of drugs on it (using hyproxic mldel of rat cerebral synaptosomes)Ca^<2+> influx through voltage-dependent Ca channel by K^+ depolarization is greater in a hypoxic group than in a control group. More than 10 uM nitrandipine, a dihydropyridune-derivative Ca antagonist, depressed this Ca^<2+> influx. However, pentobarbital failed to inhibite Ca^<2+> influx through voltage-dependent Ca channel.2) Effects of volatile anesthetics on the [ ^3H]nitrendipine binding to rat cerebral synaptic membraneVolatile anesthetics such as halothane, isoflulene and enflulene had Ca antagonist-like activity (dyhydropyridine-derivative like activity) and their potencies were in order to their anesthetic potencies.3) Effects of lidocaine-induced convulsion on c-fos protein (c-Fos) expression in rat brainConvulsions cause cell damage due to a local ischemia. C-Fos is a transcriptional modulator and is induced by intracellular Ca^<2+> increase. C-Fos expression is suggested to be a good marker of the increase in cerebral metabolism and cellular plastic change. The c-Fos expression in nemrons of the hippocampus following lidocaine-induced convulsion was quite weak, while that following convulsions induced by non-anesthetic convulsant agents such as pentylenetetrazol, kainic acid, electroconvulsive shock was strong. Scatterd, however, more intense than that in hippocampal area, the exprossion of c-Fos was observed in amygdala and pyriform lobe following lidocatine-induced convulsion. This expression was deptessid by MK-801, a NMDA antagonist.