| Project/Area Number |
16500265
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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 |
Neurophysiology and muscle physiology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
ISHIBASHI Hitoshi Kyushu University, Graduate School of Medical Sciences, Assistant Professor, 大学院・医学研究院, 講師 (50311874)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | presynaptic nerve terminal / depolarization / calcium release / glycine / neuroscience / physiology / カルシウムチャネル / 神経伝達物質 / 細胞内カルシウム / パッチクランプ / リアノジン受容体 / パッチクランプ法 / 機械的単離神経細胞 |
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| Research Abstract |
The effect of potassium-induced presynaptic depolarization on spontaneous postsynaptic currents under extracellular Ca^<2+>-free conditions was investigated in mechanically dissociated rat spinal cord neurons using whole-cell patch-clamp technique. Spontaneous synaptic currents were fully inhibited by application of strychnine, indicating that they were glycinergic inhibitory postsynaptic currents (IPSCs). Elevating extracellular K^+ concentration reversibly increased that frequency of spontaneous IPSCs even in the absence of extracellular Ca^<2+>. Tetrodotoxin had no effect on the potassium-induced synaptic potentiation. The potassium-induced increase in IPSC frequency was also observed in the absence of extracellular Na^+. However, the recovery from the synaptic potentiation was markedly inhibited in the Na^+-free conditions. The potassium-induced facilitation of spontaneous IPSCs was prevented by depletion of intracellular Ca^<2+> store with thapsigargin, suggesting the contribution of Ca^<2+>-release from intracellular Ca^<2+> stores.
These results reveal a novel mechanism by which potassium-induced depolarization regulates the intracellular Ca^<2+> concentration and exocytosis in presynaptic nerve terminals.
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