| Project/Area Number |
09460134
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
HABARA Yoshiaki Hokkaido Univ., Grad. Sch. Vet. Med., Prof., 大学院・獣医学研究科, 教授 (30142813)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥8,300,000 (Direct Cost: ¥8,300,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥6,400,000 (Direct Cost: ¥6,400,000)
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| Keywords | Exocyosis / Pancreatic B cell / Adrenal chromaffin cell / Calcium ion / Lachrymal land / Mast cell / G-protein / Cell death / 画像解析 / Na^<+ / >Ca^<2+>交換輸送 / カルシウム / 副腎髄質 / 光増感物質 / スルフォローダミン / 一重項酸素 / 膵島β細胞 / 一酸化窒素 / Na^+-Ca^<2+>交感輸送体 / 膜容量 |
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| Research Abstract |
It was suggested that nitric oxide inhibits exocytosis of insulin in pancreatic B cells, by inhibiting ATP synthesis which results in prohibition of closure of KィイD2ATPィエD2 channels due to inhibition of depolarization. Photodynamic action in SALPc-loaded rat peritoneal mast cells inhibited compound 48/80-induced exocytosis of secretory granules, indicating that singlet oxygen produced by photodynamic action may interfere with exocytotic process. It was demonstrated that, in rat pancreatic B cells, NaィイD1+ィエD1/CaィイD12+ィエD1 exchanger may contribute to glucose-induced exocytotic mechanisms. It was suggested that there were different CaィイD12+ィエD1 signalling mechanisms in acinar cells and in myoepithelial cells of guinea-pig lachrymal gland, which can be triggered with different agonists. In rat adrenal chromaffin cells, cholinergic agonist-induced exocytosis correlates with the development of both intracellular signalling mechanisms and innervation, and nicotinic mechanisms seemed to precede the appearance of muscarinic mechanisms. Carbachol-induced exocytosis is inhibited by oxidative stress in pancreatic acinar cell and [CaィイD12+ィエD1], signalling process is also disturbed the stress. Inhibition by Substance P of nicotine-induced catecholamine secretion in rat chromaffin cells is noncompetitive, suggesting that substance P inhibit the function of probably NaィイD1+ィエD1 channel domain of nicotinic receptor. Neuronal death of rat cortex can be due to disturbance of [CaィイD12+ィエD1]ィイD2iィエD2 homeostasis. In mouse ileal crypt cells, activation of G-protein and ATP can induced [CaィイD12+ィエD1]ィイD2iィエD2, elevation. All these results indicate that intracellular CaィイD12+ィエD1 plays important roles in both physiological and pathological process of various cells.
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