| Project/Area Number |
07457365
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kurume University |
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Principal Investigator |
HIGASHI Hideho Kurume Univ. Sch. Med. Professor, 医学部, 教授 (10098907)
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| Co-Investigator(Kenkyū-buntansha) |
INOKUCHI Hiroe Kurume Univ. Sch. Med. Associate Professor, 医学部, 助教授 (10080558)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,000,000 (Direct Cost: ¥7,000,000)
Fiscal Year 1996: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1995: ¥4,000,000 (Direct Cost: ¥4,000,000)
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| Keywords | Brain ischemia / Hippocampal CA 1 neurons / Initial hyperpolarization / Slow depolarization / Rapid depolarization / Electrogenic Na^+ pump / ATP-sensitive K^+ channel / Necrosis / 興奮性アミノ酸受容体 / GABA受容体 / East EPSP / Fast IPSP / Slow IPSP / Muscimol / Baclofen / 興奮性アミノ酸 / Glutamate拮抗薬 / 急峻脱分極電位 / 細胞内Ca濃度 |
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| Research Abstract |
Intracellular recording techniques were used to investigate the ionic basis for the response induced by superfusion of hypoxic medium deprivated of glucose (ischemia-simulating medium) in hippocampal CA1 pyramidal neurons of the rat tissue slices. Superfusion with ischemia-simulating medium produced a stereotyped response consiting of an initial hyperpolarization, a subsequent slow depolarization and a rapid depolarization after approximately 6 min of exposure. When oxygen and glucose are readmitted after generating the rapid depolarization, the membrane potential not only repolarized, but depolarized further, reaching 0 mV approximately 5 min after readmission. In the presence of glibenclamide or tolbutamide, the initial hyperpolarizaiton was depressed by 70% from the control amplitude. The remaining hyperpolarization was depressed by BAPTA-AM,procaine, W-7 or KN-62. These results suggest that the hyperpolarization is due to activation of both ATP-sensitive K^+ channels and Ca^<2+>-de
… More
pendent K^+channels. The reversal potential of the slow depolarization obtained in TEA (20mM) using Cs acetate electrodes was +5 mV and the amplitude was depressed by CNQX or AP-5. The results suggest that the slow depolarization is, in part, due to the interstitial accumulation of glutamate. The amplitude and maximal slope of rapid depolarization were markedly decreased by reduction in either extracellular Na^+ or Ca^<2+> but not affected by CNQX and AP-5. The reversal potential obtained in TEA (20mM) using Cs acetate electrodes was shifted in a hyperpolarizing direction by a decrease in either external Na^+ or Ca^<2+> while the reversal potential was shifted in a depolarizing direction by a decrease in external C1^-. In low K^+ media, the reversal potential was not affected. The results suggest that the rapid depolarization is Na^+, Ca^<2+> and C1^- dependent. The lack of effect of low K^+ medium is probably due to the fact that [K^+] in the recording cell environment is increased by K^+ efflux consequent to depression of the electrogenic Na^+ pump activity and to the initial hyperpolarization. Less
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