1987 Fiscal Year Final Research Report Summary
Neuropharmacological study on excitatory amino acid receptors in hippocampus
Project/Area Number |
61570103
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
General pharmacology
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Research Institution | Faculty of Pharmaceutical Sciences, Osaka University |
Principal Investigator |
BABA Akemichi Fac. Pharm. Sci., Osaka Univ. Assistant Prof., 薬学部, 助教授 (70107100)
|
Co-Investigator(Kenkyū-buntansha) |
IWATA Heitaroh Fac. Pharm. Sci., Osaka Univ., Assistant Prof., 薬学部, 教授 (30028823)
|
Project Period (FY) |
1986 – 1987
|
Keywords | Hippocampus / Excitatory amino acid receptors / chloride transport / cyclic AMP / Zn結合蛋白 |
Research Abstract |
1. Excitatory amino acid receptor binding: Glutamate (glu) cysteine sulfinate, excitatory amino acid agonists, have different binding sites in synaptic membranes of rat. Cl-Dependent glu binding sites are related,to Cl-dependent sequestration of glu. Depolarization of brain slices are accompanied by a specific increase in the Cl-dependent binding sites for glu. Furthemore, cysteic acid, an excitatory sulfur amino acid, is a specific ligand for this Cl-dependent glu binding site. 2. Cyclic AMP formation in hippocampal slices: Excitatory amino acids. such as glu and cysteine sulfinate, markedly enhance the formation of cyclic AMP through their own receptors in hippocampus. Complete dependency on Cl ion indicates that Cl transport is essential for excitatory amino acid receptors-mediated stimulation of cyclic AMP formation. 3. Release of amino acid neurotransmitter: Enhancement of GAGA release by excitatory amino acids is mediated by excitatory amino acid receptors. Insulim and Zn ion specifically attenuated the stimulatory effect of cysteine sulfinate on GABA release. In addition, Zn ion specifically inhibited the release of glu from the preloaded hippocampal slices. Zn ion localized in the soluble fraction of hippocampus as proteinbound form. Excitatory amino acids, especially quisqualate, stimulated the release of Zn ion from the binding proteins.
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