| Project/Area Number |
03454126
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TACHIBANA Masao Univ.of Tokyo, Dept.of Psychol.Prof., 文学部, 教授 (60132734)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1992: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1991: ¥3,500,000 (Direct Cost: ¥3,500,000)
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| Keywords | Synapse / Neurotransmitter / Glutamate / Ca current / Na / Ca exchanger / Ca pump / Retina / Neuron / カルシウムイオン / カルシウル電流 / カルシウムチャネル / 網膜双極細胞 / 伝達物質 / 神経細胞 / 興奮性アミノ酸 / パッチクランプ |
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| Research Abstract |
To investigate the excitation-transmitter release coupling in the vertebrate central nervous system, ON-type bipolar cells dissociated from the goldfish retina were used because these cells have an extraordinarily large presynaptic terminal. The Ca current and the intracellular free Ca^<2+> concentration ([Ca^<2+>]_i) were simultaneously monitored. Since the leading candidate for the transmitter is glutamate, the transmitter release was detected electrophysiologically by the neuron, which was highly sensitive to glutamate.
The Ca channel was identified as the high-voltage activated, dihydropyridine-sensitive type, and was highly localized to the presynaptic terminal. The basal level of [Ca^<2+>]_i in the presynaptic terminal was determined by a balance between the leakage influx of Ca^<2+> through Ca^<2+> channels and the extrusion of Ca^<2+> by the plasma membrane Ca^<2+> pump. Activation of the Ca^<2+> current evoked the Ca^<2+> transient. Its peak level seemed to be regulated by endogenous Ca^<2+> buffers. The increased [Ca^<2+>]_i recovered to the basal level due to the extrusion of Ca^<2+> by the Na^+/Ca^<2+> exchanger and the Ca^<2+> pump in the plasma membrane. Activation of the dihydropyridine-sensitive Ca^<2+> current in fact evoked the release of glutamate-like substance.
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