| Project/Area Number |
18K06701
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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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| Review Section |
Basic Section 47040:Pharmacology-related
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| Research Institution | Fukuoka University (2019-2020)
University of Miyazaki (2018) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
武谷 立 宮崎大学, 医学部, 教授 (50335981)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | アクチン重合因子Fhod3 / 樹状突起スパイン / Fhod3フォルミン蛋白質 / 神経細胞 / スパイン |
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| Outline of Final Research Achievements |
Dendritic spines in neural cells perform efficient neurotransmission by changing their morphology with reorganizing the actin cytoskeleton. However, little is known of the regulatory mechanism of the actin cytoskeleton in dendritic spines. Our present study showed that the actin polymerization factor Fhod3 is expressed in the dendritic spines of excitatory pyramidal neurons of specific regions of the cerebral cortex. A detailed analysis of spine morphology using brain-specific Fhod3-deficient mice revealed that spine maturation was inadequate compared to control mice. These findings revealed that Fhod3 is essential for spine morphogenesis of specific excitatory neurons in the cerebral cortex.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究成果は、樹状突起スパインのアクチン細胞骨格制御機構に新たな分子メカニズムを提供し得るだけでなく、スパインの形態異常を認める神経精神疾患の新たな治療法確立にむけた分子基盤となり得る。
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