| Project/Area Number |
14570044
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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 |
General physiology
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| Research Institution | Nagoya City University |
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Principal Investigator |
SUZUKI Hikaru Nagoya City University, Graduate School of Medical Siences, Professor, 大学院・医学研究科, 教授 (80037548)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Gastric smooth muscle / Spontaneous activity / Stored calcium / IP_3 / Proteinkinase C / Intracellular calcium / Mitochondria / Proton pump / 消化管平滑筋 / 歩調とり電位 / 緩電位 |
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| Research Abstract |
Recording of electrical responses from the isolated stomach muscles of the guinea-pig produced periodical generation of slow potentials with about 30 mV in amplitude and 5-6 s in duration. Slow potentials were not inhibited by TTX or Ca antagonists. Slow potentials were abolished by DIDS or niflumic acid, suggested that the potentials were produced by activation of Ca-sensitive Cl channels. Measurement of intracellular Ca concentrations by using Ca-indicator fula-2 fluorescence indicated that slow potentials were associated with an increase in intracellular Ca concentrations. Ca-responses, together with slow potentials, were inhibited by BAPTA (an intracellular Ca chilator), 2-APB (an inhibitor of IP3 receptors) and CPA (an inhibitor of internal Ca-pump). Inhibitors of mitochondrial protonophore (CCCP) or mitochondrial ATP-sensitive K-channel (5-HDA) also abolished the generation of slow potentials and Ca-transients. These results suggested that mitochondrial activity produced as a results of proton production induces an activation of Ca-sensitive enzymes and finally produces IP3, which in tern elevates intracellular Ca concentrations by releasing from the internal stores and activates Ca-sensitive ion channels at the plasma membrane. These processes are considered involved in the generation of pacemaker potentials in gastric pacemaker cells.
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