| Project/Area Number |
26430025
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Soka University |
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Principal Investigator |
Kawai Hideki 創価大学, 理工学部, 准教授 (90546243)
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| Co-Investigator(Kenkyū-buntansha) |
根本 正史 創価大学, 公私立大学の部局等, その他 (80370980)
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| Research Collaborator |
YAMASAKI Kenichi
INAKUMA Kiyonobu
NAGAYAMA Takahiro
SUZUKI Anna
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | ニコチン性受容体 / アセチルコリン / 大脳新皮質 / 聴覚皮質 / 認知症 / 知覚 / 認識 / 感覚障害 / 神経伝達 / 聴覚 / ニコチン / ムスカリン / 酵素 / 興奮性シナプス / 転写因子 / S/N比 / 神経情報処理 / 大脳皮質 / シグナル・ノイズ比 / 注意力 / 長期増強 |
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| Outline of Final Research Achievements |
Systemic nicotine exposure enhances sound evoked responses of specific auditory information while it suppresses those of non-specific information via nicotinic acetylcholine receptors in primary auditory cortex (A1). We investigated mechanisms underlying this nicotinic filtering of sensory information at molecular, cellular, and system levels. Nicotine exposure activated protein kinase A (PKA), which in turn activated extracellular signaling-regulated kinases (ERK) to confer the nicotinic filtering. Nicotine increased the amplitude of spontaneous excitatory synaptic activities via PKA by phosphorylating the subunit of main neurotransmitter glutamate-activated ion channels at or near the synapses. It was also found that nicotine suppressed the responses of inhibitory synaptic activities. These data suggest that nicotinic filtering recruits PKA to regulate both excitatory and inhibitory synapses in A1.
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