| Project/Area Number |
02670679
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Kyoto University |
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Principal Investigator |
NAKAO Shin-ichi Kyoto University, Medicine, Assistant, 医学部, 助手 (10207714)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Kenjiro Kyoto University, Medicine, Professor, 医学部, 教授 (20025620)
ARAI Toshiyuki Kyoto University, Medicine Lecture, 医学部, 講師 (80175950)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1990: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Intracellular Calcium / Cerebral Hypoxia / Calcium Antagonist / Barbiturate / c-fos / NMDA receptor / Convulsion |
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| Research Abstract |
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 membrane
Volatile 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 brain
Convulsions 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.
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