| Project/Area Number |
10680702
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | National Institute for Physiological Sciences (1999)
Kyoto University (1998) |
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Principal Investigator |
SIGEMOTO Ryuichi Natl. Inst. Physiol. Sci., Professor, 生理学研究所, 教授 (20221294)
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| Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Ayae Natl. Inst. Physiol. Sci., Research Associ., 生理学研究所, 助手 (80321610)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | glutamate / GABAB / metabotropic / receptor / cerebellum / electron microscopy / immunocytochemistry / グルタミン酸 / GABA / 受容体 / 形態学 |
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| Research Abstract |
Glutamate and GABA are major excitatory and inhibitory neurotransmitter in mammalian brain. In this research project, interaction between glutamatergic and GABAergic synapses was investigated through morphological analyses of metabotropic receptors for these neurotransmitters. In the globes pallidus and island of Calleja in the olfactory tubercle, immunogold labeling for mGluR7, a subtype of metabotropic glutamate receptors, was found in active zone of GABAergic terminals that were positive for glutamic acid decarboxylase, whereas in the cerebellum, immunogold labeling for GABABR1 and GABABR2 was found in active zone of glutamatergic terminals. P type calcium channel subunit alpha 1A, which forms voltage-gated calcium channel triggering exocytosis of glutamate was also detected in the active zone. These results indicate that excitatory and inhibitory synapses may influence each other by regulating GABA and glutmate release, respectively, from axon terminals. In the future study, we will investigate colocalization of various subtypes of receptors and calcium and other ion channels, and the mechanism of neurotransmission regulation mediated by these metabotropic receptors by electrophysiology.
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