1994 Fiscal Year Final Research Report Summary
Molecular mechanism of neural plastic changes in signal transduction, with special reference to the role of cGMP
| Project/Area Number |
04670054
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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 physiology
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| Research Institution | Tokyo Medical College |
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Principal Investigator |
KOBAYASHI Haruo Tokyo Medical College Professor of Physiology, 医学部, 教授 (20074502)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Susumu Yamaguchi University Professor of Biology, 教養部, 教授 (90022665)
MOCHIDA Sumiko Tokyo Medical College Assistant Professor of Physiology, 医学部, 講師 (30096341)
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| Project Period (FY) |
1992 – 1994
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| Keywords | Sympathetic ganglia / Synaptic trans-mission / Protein phosphorylation / G-Kinase / C-Kinase / MARCKS / Cultured neurons / Exocytosis |
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| Research Abstract |
In the present study carried out in mammalian sympathetic ganglia, it was found that 1) cyclic (c) GMP was increased in response to muscarinic stimulation, 2) cGMP induced a long-lasting depolarization, 3) G-kinase activity was detected, and 4) specific G-kinase substrate of m. w. 87K was discovered. 87K protein was identified as MARCKS which was found in the brain as a specific C-kinase sub-strate. Roles of the phosphorylation of MARCKS by G- and C-kinases were discussed in terms of slow plastic changes in ganglionic synaptic transmission.
Analyzes of endogenous functional proteins which were thought to be related to the exocytotic release of neurotransmitters were performed using de novo synapses formed between sympathetic neurons in primary culture.It was suggested that phosphorylation of non-muscle myosin II in the presynaptic terminals by myosin light chain kinase (MLCK) and subsequent interaction of myosin with actin might be involved in the process of neurotransmitter release.
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