| Project/Area Number |
12470317
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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 | NIIGATA UNIVERSITY |
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Principal Investigator |
FUJIWARA Naoshi NIIGATA UNIVERSITY Faculty of Medicine, Professor, 医学部, 教授 (70181419)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Yoko Faculty of Medicine, Assistant, 医学部, 助手 (80018853)
SEO Kenji Graduate School of Medical and Dental Sciences, Associate Professor, 大学院・医歯学総合研究科, 助教授 (40242440)
TAGA Kiichiro Graduate School of Medical and Dental Sciences, Associate Professor, 大学院・医歯学総合研究科, 助教授 (00163329)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥14,300,000 (Direct Cost: ¥14,300,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2001: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥8,400,000 (Direct Cost: ¥8,400,000)
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| Keywords | Hippocampal slices / Cortical slices / Membrane potential image / Brain ischemia / Ischemic tolerance / Oxygen-glucose deprivation / Intravenous anesthetics / Medulla slices / 脳切片 / 膨化 / 延髄 / 三叉神経脊髄路尾側亜核 / NMDA受容体 / NK_1受容体 / 神経興奮伝搬 / 脳組織切片 / 膜電位感受性色素 / 大脳皮質 / 海馬 |
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| Research Abstract |
(1) Ischemic tolerance induced by ischemic preconditioning was investigated by applying a membrane potential imaging technique to brain slices of gerbils, which were pretreated with 2-min forebrain ischemia. Excitation propagation in hippocampal slices of preconditioned animals was partially preserved, while that of untreated animals disappeared 1 day after 5-min transient ischemia. Pyramidal neurons of preconditioned animals were also preserved 2 months after the ischemic insult. The results suggest that ischemic preconditioning induced ischemic tolerance to reduce the extent of ischemic functional disturbance.
(2) Excitation propagation in brain slices, which were transiently exposed to oxygen-glucose deprivation, was examined. Evoked excitation propagation in the hippocampal CA1 and cortical layer II-III were diminished during exposure to oxygen-glucose deprivation, but partially recovered 3-5 hr after 5-min exposure to oxygen-glucose deprivation. The excitation propagation almost di
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sappeared in hippocampal slices 1 day (20-22 hr) after the exposure, while that in cortical slices was partially preserved. On the other hand, excitation propagation in both hippocampal and cortical slices, which were exposed oxygen-glucose deprivation in the presence of ketamine and thiamylal, well preserved even 1 day after the exposure. The results indicate that neuronal function in hippocampal slices more severely damaged than that in cortical slices by transient exposure to oxygen-glucose deprivation. Some intravenous anesthetics, e.g. ketamine and thiamylal, may protect neurons from oxygen-glucose depletion during ischemia.
(3) Propagation of neuronal excitation in the trigeminal subnucleus caudalis (Vc) was visualized using a high-speed optical imaging technique applied to medulla slice preparations. High frequency stimulation induced long-lasting membrane depolarization in the marginal layer, substantia gelatinosa and magnocellular layer. This excitation propagation was suppressed by MK-801 or L-703.606, suggesting that NMDA- and NK_1-receptors are involved in the nociceptive afferent transmission in Vc. Less
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