| Project/Area Number |
20570073
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Animal physiology/Animal behavior
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| Research Institution | Nagasaki University |
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Principal Investigator |
OKADA Yukio Nagasaki University, 大学院・医歯薬学研究科, 准教授 (60136687)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIYAMA Rie 長崎大学, 大学院・医歯薬学研究科, 助教 (10274664)
HOTKEZAKA Hitoshi 長崎大学, 大学院・医歯薬学研究科, 講師 (90199513)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 動物生理化学 / 細胞シグナル伝達 / 副甲状 / アラキドン酸 / Ca^<2+> / パッチクランプ / ウシガエル / イオンチャネル / 情報伝達 / Gタンパク質 |
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| Research Abstract |
Elevation of extracellular Ca^<2+> concentration induces intracellular Ca^<2+> signaling in parathyroid cells. We report the electrophysiological property associated with intracellular Ca^<2+> signaling in frog parathyroid cells and show that Ca^<2+>-activated Cl- channels are activated by intracellular Ca^<2+> increase through inositol 1,4,5-trisphophate (IP3)-independent pathway. High extracellular Ca^<2+> induced an outwardly-rectifying conductance in a dose-dependent manner. The conductance was composed of an instantaneous time-independent component and a slowly activating time-dependent component and displayed deactivating inward tail current. Extracellular Ca^<2+>-induced and Ca^<2+> dialysis-induced currents reversed at the equilibrium potential of Cl- and were inhibited by niflumic acid. Extracellular Ca^<2+>-induced currents displayed a moderate dependency on guanosine triphosphate (GTP). All blockers for phospholipase C, DAG lipase, MAG lipase and lipoxygenase inhibited extracellular Ca^<2+>-induced current. IP3 dialysis failed to induce conductance increase, but 2-AG, arachidonic acid and 12(S)-HPETE dialysis increased the conductance identical to extracellular Ca^<2+>-induced conductance. These results indicate high extracellular Ca^<2+> raises intracellular Ca^<2+> concentration through DAG lipase/lipoxygenase pathway, resulting in the activation of Cl^-conductance.
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