| Project/Area Number |
62570084
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Nippon Medical School (1988)
Tokyo Medical and Dental University (1987) |
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Principal Investigator |
MIYATA Yuhei Nippon Medical School, Professor, 医学部, 教授 (00014275)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Fumiko Nippon Medical School, Assistant Professor, 医学部, 助手 (50142526)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Plasticity / Synapse / Trophic substance / 電気的活動 / シナプス伝達 / EPSP |
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| Research Abstract |
In our previous study, it was found that IA synaptic transmission is enhanced before the depression occurs following muscle nerve section. It was hypothesised that IA synaptic transmission is regulated by electrical activity and a factor from a muscle, the former depresses the transmission while the latter enhances. In this research project, we aimed to identify the factor biochemically and to determine whether the enhancement of synaptic transmission is due to newly synthesis of proteins necessary for synaptic transmission.
Actinomycin D prevented the increase of Ia EPSPs shortly after muscle nerve section, suggesting the enhancement of Ia synaptic transmission following axotomy is due to increase of protein synthesis.
For biochemical analysis, we have begun to investigate proteins using 2 dimensional gel electrophoresis. The basic idea to identify the factor is that the factor is present in both normal muscle and nerve, but is depleted in the Ia sensory neurons of which peripheral axons are sectioned a few weeks ago.
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