| Project/Area Number |
07458218
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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 |
神経・脳内生理学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TACHIBANA Masao The Univ.of Tokyo, Grad.School of Hum.& Soc., Dept.of Psychol., Professor, 大学院・人文社会系研究科, 教授 (60132734)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Takashi The Univ.of Tokyo, Grad.School of Hum.& Soc., Dept.of Psychol., Res.Associate, 大学院・人文社会系研究科, 助手 (00242082)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 1996: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1995: ¥5,900,000 (Direct Cost: ¥5,900,000)
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| Keywords | retina / synapse / chemical transmitter / glutamate / glutamate receptor / calcium ion / calcium pump / sodium・calcium exchanger / エクソサイトーシス / カルシウムチャネル / カルシウム依存性カリウムチャネル / カルシウム依存性塩素チャネル |
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| Research Abstract |
Glutamate plays a key role in retinal synaptic transmission. Firstly, we examined Ca^<2+> buffering system in the presynaptic terminals of bipolar cells. Bipolar cells with large presynaptic terminals were isolated from the goldfish retina. The presynaptic Ca current (I_<Ca>) was measured under the whole-cell voltage clamp, and at the same time, the cytoplasmic free Ca^<2+> concentration ([Ca^<2+>]_i) in the terminal was monitored with fura-2 fluorimetry. Activation of I_<Ca> by a depolarizing pulse evoked a Ca^<2+> transient. Its peak amplitude was determined mainly by Ca^<2+> -binding substances, while its recovery was due to the extrusion of Ca^<2+> by Ca^<2+> -ATPase and Na^+/Ca^<2+> exchanger in the plasma membrane. Submembrane [Ca^<2+>]_i, which was estimated using the Ca^<2+> -activated K^+ channel as a Ca^<2+> probe, increased to >10muM upon activation of Ca^<2+> channels. Secondly, we examined the relationship between I_<Ca> and glutamate release. Glutamate release was monitored with a NMDA-receptor rich neuron or as membrane capacitance changes associated with exocytosis. Glutamate release composed of two components ; the rapid component seemed to be due to the fusion of immediately releasable synaptic vesicles, while the delayd slow component seemed to reflect the mobilization of releasable synaptic vesicles. Thirdly, using retinal slice preparation, we examined the properties of glutamate receptors in ganglion cells. Analysis of EPSPs, which were evoked spontaneously, by the electrical stimulation of bipolar cells, or by light stimulation, demonstrated that glutamate released from bipolar cells activated both NMDA and non-NMDA receptors.
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