| Project/Area Number |
08459004
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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 |
広領域
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| Research Institution | UNIVERSITY OF TSUKUBA |
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Principal Investigator |
KURAMOTO Taketeru INSTITUTE OF BIOLOGICAL SCIENCES,UNIVERSITY OF TSUKUBA,ASSOCIATE PROFESSOR, 生物科学系, 助教授 (40015813)
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| Co-Investigator(Kenkyū-buntansha) |
YAZAWA Tohru DEPARTMENT OF SCIENCES,TOKYO METROPOLITAN UNIVERSITY,ASSISTANT PROFESSOR, 理学部, 助手 (30106603)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥5,500,000 (Direct Cost: ¥5,500,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥4,000,000 (Direct Cost: ¥4,000,000)
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| Keywords | Ca^<2+> channels / Cardiac muscle / Crustaceans / G proteines / Membrane properties / Pericardial peptides / Spiny lobster / Temperature / 甲殻十脚類 / イオンチャネル / カルシウムイオン / G タンパク質 / 心臓 / カリウムイオン |
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| Research Abstract |
Crustacean cardiac muscles often generate graded action potentials (spikes) on excitatory junction potentials (EJPs). Amplitude of the spikes increased in proportion to falling temperature in myocardial cells of Panulirus japonicus. We have supposed that falling temperature causes inward Ca^<+2> currents to increase by activation of Ca^<+2> channels of the myocardial membrane. This hypothesis was examined in the nerve-muscle preparations of the lobster heart. The muscle membrane currents were analyzedwith the voltage clamp method.
The muscle inward currents were divided into rapid currents corresponding to the spikes ; slow currents to the EJPs and sustained currents induced by cooling. The former easily disappeared and the latter two hardly did with an application of Co^<+2> (10-20 mM). Tetraethylammonium (TEA : a K^+ channel blocker) increased the falling rate of spike. But cooling did it more. Therefore, the graded increase of inward currents may be partly attributed to depression of the outward K^+ currents, but the cold-induced spiking cannot be explained only by suppression of the K^+ channels. The inward rapid currents were blocked by nifedipine (20 mM) and also pertussis toxin (PTX). These data suggest that the myocardial membrane has L-type Ca^<+2>channels and that PTX-sensitive GTP-binding proteins (G proteins) may concern the cold-inducing Ca2+currents. When the G protein subunits, GDP-beta-S and GTP-gamma-S, were injected into the myocytes, the GTP-gamma-S enhanced the Ca^<+2> currents and the GDP- beta-S reduced them. Peptide components of the pericardial hormones (F1 and proctolin) often induced the spikes again in the preparation abolishing them. Therefore, the pericardial peptides may activate the G proteins. Then the cold dependent increase of Ca^<+2> currents may be resulting from cold depression of G protein-mediated closing of the Ca^<+2>channels.
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