| Project/Area Number |
63480476
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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 |
応用薬理学・医療系薬学
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| Research Institution | Osaka University |
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Principal Investigator |
IWATA Heitaroh Osaka Univ.. Pharmaceutical Sci. Professor, 薬学部, 教授 (30028823)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUDA Toshio Osaka Univ.. Pharmaceutical Sci. Research Assistant, 薬学部, 助手 (00107103)
BABA Akemichi Osaka Univ.. Pharmaceutical Sci. Assistant Professor, 薬学部, 助教授 (70107100)
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| Project Period (FY) |
1988 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1988: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | Chloride ion / Hippocampus / Excitatory Amino Acid / cyclic AMP / adenylate cyclase / astrocyte / swelling / 蛍光プロ-ブ / 蛍光プローブ / ストップトフロー |
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| Research Abstract |
1.C1^--Dependent cyclic AMP formation : Cyclic AMP formation in hippocampal slices by excitatory amino acid and that by norepinephrine in cultured astrocytes were dependent on extracellural C1^-. C1^- transport blockers inhibited the cyclic AMP formation. The action site of C1^- was suggested to be the catalytic sub-unit in receptor-coupled adenylate cyclase systems. These results indicates that C1^- is an important factor in intracellular signal transーduction systems.
2.C1^--Dependent glutamate transport : Cysteic acid was shown to be a selective substrate of the C1^--dependent glutamate transporter in synaptic membranes. And cystic acid transport was suggested to be coupled with C1^- transport, but not with Na^+ transport. The glu-tamate transport activity was increased by neuronal activity and in some brain Pathdogical states such as ischemia.
3.Glutamate-induced swelling of astrocytes : We found that the glutamate-induced swelling of cultured astrocytes is dependent on extracellular Ca^<2+>r and C1^- and published them. Ca^<2+> and C1^- transport inhibitors prevented the swelling. The ultrastructural changes in swollen astrocytes have similar properties to that swollen in brain disorders, suggesting a pathological significance of glutamate-induced excessive C^- influx into astrocytes.
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