| Project/Area Number |
61570887
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
TSUJIMOTO Akira Hiroshima University School of Dentistry, Professor, 歯学部, 教授 (90034181)
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| Co-Investigator(Kenkyū-buntansha) |
DOHI Toshihiro Hiroshima University School of Dentistry, Associate Professor., 歯学部, 助教授 (00034182)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1987: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1986: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Mucin / Submandibular gland / Ca^<2+> / Acetylcholine / Norepinephirne / Dog / ムチン分泌 / 単離腺房細胞 / α受容体 / β受容体 / カルシウムcAMP / 腺房細胞 / cyclic AMP |
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| Research Abstract |
Adrenergic and cholinergic stimulation of mucin release and the role of Ca^<2+> have been investigated in the isolated dog submandibular gland cells.
Stimulation of muscarinic cholinergic, alpha-adrenergic and beta-adrenergic receptors elicited mucin release from dispersed dog submandibular gland cells. The secretory response to ACh was much pronounced than those to adrenergic agonists, and largely dependent on the presence of extracellular Ca^<2+>, but the dependency on the extracellular Na^+ was slight. Ionomycin also stimulated mucin release from the cells. Neither muscarinic cholinergic agonists nor ionomycin were effective mucosecretagogues as beta-adrenergic agonists in rat submandibular gland cells. Alpha-adrenoceptor-mediated release was decreased by chelating extracellular Ca^<2+> with EGTA. Beta-adrenoceptor-mediated response was diminished by extensive exposure of cells to EGTA, due at least in part to the requirement of Ca^<2+> for beta-adrenoceptor stimulation of cAMP formation. 8-br-cAMP stimulated ^<45>Ca^<2+> release from the cells preloaded with ^<45>Ca^<2+>.8-br-cAMP-induced mucin release was eliminated in ionomycin-pretreated cells, but not inhibited by chelating extracellular Ca^<2+> and by the treatment of the cells with TMB-8 or in the cells loaded with BAPTA. These results suggest that not only adrenergic system but also muscarinic cholinergic system may participate in the regulation of mucin release in dog submandibular gland, and also provide the possibility that, in addition to cAMP mediated mechanism, Ca^<2+>-dependent mechanisms may be involved in the mucosecretion in dog submandibular acini.
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