1992 Fiscal Year Final Research Report Summary
Regulation of glutamate neurotransmission by endogenous Zn^<++>
| Project/Area Number |
02454136
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
BABA Akemichi Osaka Univ., Fac. Pharm.Sci. Professor, 薬学部, 教授 (70107100)
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| Co-Investigator(Kenkyū-buntansha) |
KOYAMA Yutaka Osaka Univ. Fac. Pharm.Sci. Research Associate, 薬学部, 助手 (00215435)
MATUDA Toshio Osaka Univ. Fac. Pharm.Sci. Associate Professor, 薬学部, 助教授 (00107103)
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| Project Period (FY) |
1990 – 1992
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| Keywords | Glutamate / Zn^<++> / NMDA receptor / Protein kinase C / astrocyte / swelling |
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| Research Abstract |
1.Effect of L-glutamate on Zn^<2+> binding protein: We found a Zn^<2+> binding protein in cytosolic fraction of rat hippocampus. L-glutamate and its analogues stimulated the dissociation of Zn^<2+> form the protein. Chronic application of a Zn^<2+> chelator, dithizone, into rat hippocampus decreased the level of L-glutamate but not those of the other transmitters.
2.Translocation of protein kinase C (PKC) : In hippocampla synaptoneurosome, NMDA and L-glutamate induced translocation of PKC from cytosol to plasma membrane. The NMDA-induced translocation was dependent on Ca^<2+> and required for trace amount of endogenous Zn^<2+>. The effect of NMDA showed a developmental changes, where the effect was most obvious at 7 day from the birth.
3.Regulation of L-glutamate release: Zn^<2+> inhibited release of L-glutamate, but not those of GABA and acethycholine, from hippocampal slices, while dithizone increased the L-glutamate release.
4.Inhibition of PI turnover: The inhibition of NMDA on carbachol-induced PI(phosphatidilinositol) turnover was suppressed by Zn^<2+> The effect was caused by inhibition of Ca^<2+> influx by Zn^<2+>.
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