Project/Area Number |
11670622
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Osaka University |
Principal Investigator |
UEDA Hirokazu Osaka University Graduate School of Medicine, Osaka University, Lecturer, 医学系研究科, 講師 (10294117)
|
Co-Investigator(Kenkyū-buntansha) |
SEIYAMA Akitoshi Osaka University Graduate School of Medicine, Osaka University, Assistant Professor, 医学系研究科, 助手 (70206605)
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
Keywords | Cerebral ischemia / Energy Metabolism / Neuronal death / Immunohistochemistry / Mitochondria / N-acetylaspartate / vasoreactivity / Selective Vulnerability / Immunohistochemisty |
Research Abstract |
We showed the role of mitochondrial dysfunction in the pathogenesis for selective vulnerability in hypoxic/ischemic brain damage, as follows. 1. We developed the methods for simultaneous assessment of immunohistochemical damages and changes in regional metabolite levels in the brain tissue with 10-50μg dry weight. In the selectively vulnerable areas such as CA1 area of the hippocampus and layer III/IV of the cerebral cortex, recovery of high-energy phosphate levels was delayed from the ischemic insults, as compared to that in the less-vulnerable areas. The result indicated that a slight impairment of mitochondrial dysfunction during ischemia and reperfusion period could lead to extensive neuronal damages. 2. Ischemic periods necessary for development of arteriolar vasoconstriction and energy failure were very close to each other, indicating that mitochondrial dysfunction affected vasoreactivity in gerbil model of cerebral ischemia. 3. Decrease of N-acetyl-aspartate level was observed in the selectively vulnerable regions after ischemia. NAA level seemed an useful index for neuronal survival.
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