| Project/Area Number |
10680747
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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 |
Neuroscience in general
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| Research Institution | Oita Medical University |
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Principal Investigator |
ISONO Mitsuo Oita Medical University, Dept. of Neurosurgery, Assistant Professor, 医学部, 講師 (60151437)
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| Co-Investigator(Kenkyū-buntansha) |
磯野 光夫 大分医科大学, 医学部, 講師 (60151437)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Neuronal death / microglia / gliosis / apoptosis / impact-acceleration injury / NMDA / AMPA / neuronal death / astrogliosis / TGFα / apoptosis / アストロサイト / マイクログリア |
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| Research Abstract |
We investigated the effects of TGF on cellular responses and histological findings after traumatic brain injury in rats. The topical application of TGF-∂ enhanced inductions of microglial cells and reactive gliosis. On the other, TGF-βreduced microglial proliferations. We are further planning to develop a new model using transgenic mice which can overexpress TGF-∂.
We also developed the impact-acceleration injury model of rats. In this model, relative constant neuronal degeneration were found in dorsal brain stem axonal injuries in cingulum bundle and in pyramidal tract. These neuronal damages did not associate with apoptotic procedure and findings of primary DNA damages. The secondary regeneration by deafferentation was investigated in cerebellum and thalamus that have close connection with rostral brain stem. No neuronal damages were found in cerebellum, but in thalamus relatively delayed neuronal degenerations were common. Interestingly, both NMDA and AMPA/Kinate subclass of glutamate receptor antagonists reduced these neuronal damages.
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