2001 Fiscal Year Final Research Report Summary
Gene and Protein Analysis on Ischemic Tolerance Caused by Focal Brain Lesioning
| Project/Area Number |
12671352
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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 | Mie University |
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Principal Investigator |
KAWAGUCHI Kenji Mie University, Hospital, Research Associate, 医学部・附属病院, 助手 (90303742)
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| Co-Investigator(Kenkyū-buntansha) |
TAKI Waro Mie University, Faculty of Medicine, Professor, 医学部, 教授 (70144368)
HORI Kotaro Mie University, Faculty of Medicine, Research Associate, 医学部, 助手 (10303728)
MATSUSHIMA Satoshi Mie University, Hospital, Assistant Professor, 医学部・附属病院, 講師 (50252367)
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| Project Period (FY) |
2000 – 2001
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| Keywords | brain protection / brain ischemia / focal brain lesioning / GLT-1 / GluR2 / bcl-2 |
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| Research Abstract |
Deep prepiriform cortex (DPC) is the modulatory site for ischemic brain injury. We studied the mechanism on the gene and the protein expression about glutamate transporters (GLT-1, GLAST, EAAC-1), calcium ion non-permeable glutamate receptor subunit (GluR2) and apoptosis relating factors (bcl-2, bax) in the brain after DPC destruction. The major findings of this study are (1) Gene and protein expression in GLT-1, GluR2 and bcl-2 increased at the hippocampus and cortex after DPC destruction, however GLAST, EAAC-1 and bax were unchanged, (2) Gene and protein expression in GLT-1, GluR2 and bcl-2 increased at the hippocampus and cortex after ischemia in the DPC-destructed brain, and (3) The number of viable cell in the hippocampus increased in global ischemia and the volume of infarction in the cortex in focal ischemia in the DPC-destructed brain. Therefore up-regulation of GLT-1, GluR2 and bcl-2 each leads to increase of glutamate uptake, low calcium ion permeability and anti-apoptosis, then result in brain protection for ischemia.
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Research Products
(10 results)
