| Project/Area Number |
14540630
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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 |
動物生理・代謝
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| Research Institution | Nagasaki University |
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Principal Investigator |
OKADA Yukio Nagasaki Univ., Sch.Biomedical Sci., Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (60136687)
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| Co-Investigator(Kenkyū-buntansha) |
TODA Kazuo Nagasaki Univ., Sch.Biomedical Sci., Professor, 大学院・医歯薬学総合研究科, 教授 (80134708)
MIYAZAKI Toshihiro Nagasaki Univ., Sch.Biomedical Sci., Research Associate, 大学院・医歯薬学総合研究科, 助手 (10174161)
HOTOKEZAKA Hitoshi Nagasaki Univ., Sch.Biomedical Sci., Lecturer, 大学院・医歯薬学総合研究科, 講師 (90199513)
MIYAMOTO Takenori Japan Women's Univ, Fac.Sci., Associate Proflesor, 理学部, 助教授 (10167679)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Parathyroid / Arachidonic acid / Ca^<2+> / Patch-clamp / Bullfrog / Ionic channel / Signal transduction / G protein / 上皮小体 / イオンチャネ |
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| Research Abstract |
Extracellular Ca^<2+> regulates the secretion of PTH from mammalian parathyroid cells through extracellular Ca^<2+>-sensing receptor(CaR). The transduction mechanism on the Ca^<2+>-sensing was investigated using the electrophysiological technique. Parathyroid cells were isolated from the parathyroid glands of bullfrogs. Under whole-cell mode with standard K^+ internal solution, frog parathyroid cells displayed resting potential of -30±2 mV (N=44). The mean input resistance and membrane capacitance were 13.7±0.9 GΩ and 7.6±0.2 pF, respectively. After attaining the whole-cell configuration in normal saline solution, almost all frog parathyroid cells displayed transient inward currents in response to depolarizing voltage steps from a holding potential of -84 mV. The inward currents disappeared by the replacement of external Na^+ with NMDG^+ and were reversibly inhibited by TTX, indicating that the currents occur through the TTX-sensitive voltage-gated Na^+ channels. When external Ca^<2+> level was increased from 1.8 to 10 mM, the parathyroid cells displayed a large increase in conductance. The reversal potential of the response shifted according to internal Cl^- concentration. The dialysis of 0.8 mM Ca^<2+> into the cells also induced niflumic acid-sensitive conductance. The extracellular Ca^<2+>-induced currents were strongly inhibited by external Gd^<3+> and intracellular U-73122. Intracellular dialysis of IP_3 did not elicit any response in the parathyroid cells, but the dialysis of ETYA induced large inward currents. The results suggest that extracellular Ca^<2+> rise elicits Ca^<2+>-activated Cl^- conductance in frog parathyroid cells through the arachidonic acid cascade.
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