| Project/Area Number |
13671458
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Jichi Medical School |
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Principal Investigator |
MASUZAWA Toshio (2002) Jichi Medical School, School of Medicine, Professor, 医学部, 教授 (60049038)
小黒 恵司 (2001) 自治医科大学, 医学部, 講師 (90231232)
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| Co-Investigator(Kenkyū-buntansha) |
増沢 紀男 自治医科大学, 医学部, 教授 (60049038)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | IP_33kinase / IP4 / knock-out mouse / global ischemia / hippocampus / passive avoidance / gap junction / connexin / neural connexins / Cx32 knock-out |
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| Research Abstract |
Functional changes in IP_33kinase knock-out mice
To investigate the role of IP4 in the normal or the pathological conditions, we performed experiments using IP_33kinase knock-out mice. The vulnerability to global ischemia by 10 min bilateral common carotid occlusion, no differences was detected in pathological study between knock-out mice and the wilt type. Calcium increase in Rhod2 imaging induced by oxygen-glucose deprivation on hippocampal slice also showed no differences. In passive avoidance test IP_33kinase knock-out mice showed significantly poorer results. These results suggest that IP4 plays some role in keeping memory.
The role of gap junction in cerebral ischemia
The present study was undertaken to examine the hypothesis that the gap junctional proteins Cx (connexin) 32 (expressed by oligodendrocytes and/or interneurons), Cx36 (expressed by interneurons and some pyramidal neurons) and Cx43 (expressed by astrocytes) play a role in defining cell-specific patterns of neuronal deat
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h in the hippocampus after global ischemia in mice. Global ischemia did not significantly alter Cx32, Cx36 and Cx43 mRNA expression in the vulnerable CA1, as assessed by Northern blot analysis and in situ hybridization. Global ischemia induced a selective increase in Cx32 and Cx36, but not Cx43, protein abundance in CA1 prior to the onset of neuronal death, as assessed by Western blot analysis. The increase in Cx32 and Cx36 expression was in palvalbumine positive inhibitory interneurons of the hippocampal CA1, as assessed by double immunofluorescence. Abundance of the three connexin proteins was unchanged in CA3 and dentate gyrus at all times examined. The finding that connexin proteins change in the absence of a change in the corresponding mRNAs is consistent with the regulation of Cx32 and Cx36 expression at the translational and/or post-translational levels. Cx32 (Y/) null mice exhibited enhanced vulnerability to brief ischemic insults, consistent with a role for Cx32 gap junctions in neuronal survival. These findings suggest a mechanism by which Cx32 and Cx36 gap junctions contribute to the survival and resistance of GABAergic interneurons, thereby defining cell-specific patterns of global ischemia-induced neuronal death. Less
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