| Project/Area Number |
15K18382
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Aoyama Gakuin University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | グリシン受容体 / シナプス可塑性 / CaMKII / ゼブラフィッシュ / マウスナー細胞 / 抑制性シナプス / Gephyrin |
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| Outline of Final Research Achievements |
Glycinergic synaptic transmissions on a Mauthner cell (M-cell) are potentiated following repetitive exposure to acoustic stimuli. However, the molecular basis has not been elucidated. In this study, I used fluorescent protein tagged glycine receptor (Venus-GlyR) expressing M-cells of larval zebrafish as model cells to reveal the molecular basis. The M-cells enable to visualize synaptic accumulation of Venus-GlyR as a change in the fluorescent intensity. The present study revealed that synaptic GlyR clusters on a M-cells enlarge following persistent acoustic stimuli. Further efforts uncovered that CaMKII-dependent phosphorylation of gephyrin, scaffolding protein of inhibitory synapse, increases the binding affinity between gephyrin and GlyR. Our findings suggest that GlyR clustering enhancement driven by the gephyrin phosphorylation is a key mechanism of potentiation of glycinergic synaptic transmissions on a M-cell that was induced by the repetitive acoustic stimulation.
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