| Project/Area Number |
63440054
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Teikyo University School of Medicine |
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Principal Investigator |
TAMURA Akira Teikyo Univ. Neurosurgery, Prof., 医学部, 教授 (80111532)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIE Waki Teikyo Univ., Neurosurgery, Assis, 医学部, 助手 (90228966)
NAKAYAMA Hitoshi Teikyo Univ., Neurosurgery, Assis. Prof., 医学部, 講師 (00147050)
TOMUKAI Noriko Teikyo Univ., Neurosurgery, 医学部, 教務職員 (30192214)
GOTOH Osamu Teikyo Univ., Neurosurgery, Assis. Prof., 医学部, 講師 (40134598)
KIRINO Takaaki Teikyo Univ., Neurosurgery, Asso. Prof., 医学部, 助教授 (10161605)
高木 清 帝京大学, 医学部, 講師 (40197059)
水野 重樹 帝京大学, 医学部, 助手 (60200010)
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| Project Period (FY) |
1988 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥25,300,000 (Direct Cost: ¥25,300,000)
Fiscal Year 1991: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 1990: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 1989: ¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1988: ¥10,700,000 (Direct Cost: ¥10,700,000)
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| Keywords | rat / focal cerebral ischemia / neurotransmitter / memory / degeneration / thalamus / substantia nigra / アスパラギン酸 / MKー801 / 迷路学習 / 黒質 / 視床 / 脳血流量 / 脳グルコース代謝 |
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| Research Abstract |
Recently, the potential role of neurotransmitters on ischemic neuronal injury has come to be widely realized. In particular, the role of excitatory amino acids neurotransmitters, such as glutamate and aspartate, atracts attention. In this study, we examined neuronal alterations in a chronic phase after focal cerebral damage, changes of neurotransmitters after ischemia, the effect of a non-competitive antagonist of excitatory amino acid receptor, MK-801, on focal cerebral ischemia model in rats, and behavioral changes after focal cerebral ischemia. In the neuropathological study, we particularly focused on the delayed changes in the ipsilateral thalamus and also those in the ipsilateral substantia nigra. In the rat MCA occlusion model, marked atrophic chenges were obserbed in the ipsilateral thalamus and also ipsilateral substantia nigra at 6 months following MCA occlusion. The degeneration and shrinkage of these areas on the ischemic side is most likely due to neurotransmitter-mediated
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cell death. These results show the delayed neuronal loss in the distant, non-ischemic areas after focal cerebral ischemia. These neuropatholocgical changes in the ipsilateral thalamus and substantia nigra initially found in the rat MCA occlusion model similarly occurred in clinical cases of cerebral infraction in the MCA territory. Secondary, we examined the effect of MK-801 on focal cerebral ischemia model. Consequently, the area of infraction in the cerebral cortex was significantly decreased in the treated group. The results show that the excitotoxic mechanism may be responsible for ischemic injury in the cortical neurons. Thirdly, we studied behavioral changes after focal cerebral ischemia in rats. The MCA-occluded animals showed a significant impairment of learning behavior compared to the sham-operated animals in the one trial passive avoidance response and also active avoidance response. In the active avoidance task, the the learning impairment closely correlated with tissue damage, although the correlation was not observed in the passive avoidance task. Less
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