1993 Fiscal Year Final Research Report Summary
Synaptic up-and down-regulation by changes in intracellular calcium concentrations
| Project/Area Number |
04670072
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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 |
科学技術史(含科学社会学・科学技術基礎理論)
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
KATO Nobuo Kyoto Univ.Fac.Med., Instructor, 医学部, 助手 (10152729)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Synaptic plasticity / LTP / LTD / Calcium / Cortex |
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| Research Abstract |
Glutamate is the major excitatory neurotransmitter in the cerebral cortex. After blockade of NMDA and non-NMDA ionotropic glutamate receptors, tetanization to presynaptic fibers were induced long-term depression. Further experiments with agonists and antagonists suggested that some G protein-linked, inositol-1,4,5-trisphosphate (IP3)-coupled types of metabotropic glutamate receptors (mGluRs) are involved in induction of this long-term depression. Intracellular injection of the G-protein inhibitor GDPbetaS or the IP3 receptor inhibitor heparin prevented long-term depression but allowed long-term potentiation induction. Also Ca^<2+> chelation by EGTA prevented long-term depression. These experiments suggest that Ca^<2+> released from cytosolic stores resulted in long-term depression, whereas Ca^<2+> influxes lead to long-term potentiation. It thus seems that Ca^<2+> source may determine the whole fate of synaptic regulation.
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