| Project/Area Number |
06404066
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIDA Hajime The Univ.of Tokushima, Sch.of Dentistry, Professor, 歯学部, 教授 (70028364)
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| Co-Investigator(Kenkyū-buntansha) |
SKOWRONSKI Mariusz The Univ.of Tokushima, Sch.of Dentistry, Research Associate, 歯学部, 助手 (00294702)
EGUCHI Takafumi The Univ.of Tokushima, Sch.of Dentistry, Research Associate, 歯学部, 助手 (90263847)
ISHIKAWA Yasuko The Univ.of Tokushima, Sch.of Dentistry, Associate Professor, 歯学部, 助教授 (40144985)
天野 伊知郎 徳島大学, 歯学部, 助手 (20212566)
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| Project Period (FY) |
1994 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥24,800,000 (Direct Cost: ¥24,800,000)
Fiscal Year 1997: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1996: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1995: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1994: ¥16,500,000 (Direct Cost: ¥16,500,000)
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| Keywords | Salivary glands / Cell surface receptors / Supersensitivity / Desensitization / GTP binding proteins / Phosphorylation / Dephosphorylation / Okadaic acid / 40KDa蛋白質 / 34KDa蛋白質 / 老化 / 細胞増殖 / イソプロテレノール / 核蛋白質 / ヒストン蛋白質 / 非ヒストン蛋白質 / 唾液分泌 / 感作 / 脱感作 / 受容体 / G蛋白質 |
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| Research Abstract |
The functional alterations of cell surface receptors cause the changes of G protein functions and of cellular responses. In this study, we investigated the mechansims underlying the alterations of cell responses of salivary glands induced by beta agonists, acetylcholine or histamine, and the age-dependent changes in the cell proliferation of the glands of rats treated with beta agonists, and obtained the results as follows.
(1) Treatment for 30min of saliary glands with isoproterenol (IPR) or histamine resulted in the desensitization of salivary secretion in response to the agonist. The treatment for less than 10min with IPR caused conversely the supersensitivity of the secretion, but that with histamine did not.
(2) The enhancement and the suppresion of Gi protein functions were coupled with the desensitization and the supersensitivity induced by IPR,respectively. But the changes in Gs protein functions were not observed in the tissues caused the desensitization or the supersensitivity. Immunoblot analyzes with AS/7 and RM/1 demonstrated that the levels of Gi2alpha and Gsalpha proteins were not modified by beta_2 agonist- or histamine- treatment.
(3) The decrease and the increase in the phosphorylation of Gi2alpha protein coupled with the desensitization and the supersensitivity of amylase secretion by IPR,respectively. Pretreatment of the tissues with okadaic acid at the concentrations to inhibit protein phosphatase2A activity completely blocked the enhancement of Gi2alpha protein function and resulted in the disappearance of the desensitization or in the enhancement of the supersensitivity.
(4) The changes in the secretory responses of the glands to beta_2 agonists or acetylcholine after birth paralleled with those in the neurotransmitter receptor and in the function of G proteins.
(5) The time required to initiate DNA synthesis in the glands after IPR administration increased significantly with age and the level of DNA synthesis decreased markedly till 16 weeks old.
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