1989 Fiscal Year Final Research Report Summary
An electrophysiological study on miniature Ca relelase from the sarcoplasmic reticulum in cardiac myocytes.
Project/Area Number |
63570040
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
General physiology
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Research Institution | Saga Medical School (1989) Kyushu University (1988) |
Principal Investigator |
EHARA Tsuguhisa Saga Medical School, Dept. of Physiology Professor, 医学部, 教授 (50037446)
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Co-Investigator(Kenkyū-buntansha) |
ONO Kyoichi Kyushu Univ., Faculty of Medicine Dept. of Physiology, Assistant, 医学部, 助手 (70185635)
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Project Period (FY) |
1988 – 1989
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Keywords | Ca^<2+>-mediated ion channel / sarcoplasmic reticulum / whole cell recording / caffeine / Ca release |
Research Abstract |
Abstract. In order to examine the effects of increased intracellular Ca^<2+> level on the membrane electrical activity, caffeine, the agent which facilitates Ca^<2+> release from the sarcoplasmic reticulum, was applied to single ventricular cells of the guinea-pig, under condition of the whole cell recording. Caffeine (10 - 25 mM) induced a burst of pulse-like small inward currents. The amplitude of the pulse-like inward currents, which appeared to have a unit magnitude, decreased as the membrane was depolarized, and the reversal potential was estimated to be near 0 mV. Thus, the responsible ion channel may have a unit conductance of 250 - 300 pS. The pulse-like activity persisted when external NaCl was replaced with LiCl, but it disappeared in Tris-Cl solution. Large depolarizations producing sustained cell shortening or intracellular Ca^<2+>-injection enhanced the pulse-like events, suggesting a role of intracellular Ca^<2+> in this phenomenon. Ni^<2+> ions partially inhibited the pulse-like activity. Thus, the ventricular cells appeared to have Ca^<2+>-mediated cation channels with a large conductance, but possible involvement of a specific action of caffeine in the channel activation was not excluded.
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