1993 Fiscal Year Final Research Report Summary
Mechanisms of Neurotransmitter Release in the Central Nervous System
| 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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| Keywords | Synapse / Neurotransmitter / Glutamate / Ca current / Na / Ca exchanger / Ca pump / Retina / Neuron |
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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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