1995 Fiscal Year Final Research Report Summary
Neuropharmacological studies on the roles of glial receptors for neurotransmitters in gliosis
| Project/Area Number |
05454149
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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.of Pharmaceutical Sciences, Prof., 薬学部, 教授 (70107100)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Hitoshi Osaka Univ., Fac.of Pharmaceutical Sciences, Assistant, 薬学部, 助手 (30240849)
KOYAMA Yutaka Osaka Univ., Fac.of Pharmaceutical Sciences, Assistant, 薬学部, 助手 (00215435)
MATSUDA Toshio Osaka Univ., Fac.of Pharmaceutical Sciences, Associate Prof., 薬学部, 助教授 (00107103)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Gliosis / Astrocyte / Glutamic acid / Endothelins / Prostaglandins / Na, K-ATPase / IGF-I / Brain injury |
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| Research Abstract |
It is considered that glial cells have a role in brain injury, but exact mechanism is not known. In this project, the studies on receptors (glutamate, endothelins and prostaglandins) , glutamate transporter and Na^+, K^+-ATPase were carried out, in order to clarify the physiological and pathological roles of glial cells in brain. The following results were obtained.
1. In cultured rat astrocytes, glutamate caused swelling and taurine release. The swelling was mediated via ionotropic glutamate receptors and glutamate transporters.
2. Inhibitors of glutamate transporter interacts with metabotropic glutamate receptors in astrocytes.
3. Endothelins caused a morphological change in cultured astrocytes. Our studies demonstrate that the peptides modulate cytoskeletal protein organization via a small G protein.
4. Endothelin in vivo increased the number of GFAP-positive cells in rat brain.
5. Structure and expression of prostaglandin F2a and thromboxane A2 receptors were clarified in astrocytes.
6. IGF-I caused a isoform-specific induction of Na^+, K^+-ATPase in cultured astrocytes. The induction may be involved in the mitogenic action of the peptide on astrocytes.
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