| Project/Area Number |
16K18366
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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 |
Neurophysiology / General neuroscience
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| Research Institution | Tohoku Medical and Pharmaceutical University |
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Principal Investigator |
YAMAMOTO Yui 東北医科薬科大学, 医学部, 助教 (80635087)
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| Research Collaborator |
OWADA Yuji
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | FABP3 / FABP / GAD67 / GABA / 抑制性介在神経 / 抑制性介在ニューロン |
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| Outline of Final Research Achievements |
In this study, we show that FABP3 is strongly expressed in the GABAergic inhibitory interneurons of the mouse anterior cingulate cortex (ACC). Interestingly, FABP3 KO mice show an increase in the expression of the gene encoding the GABA-synthesizing enzyme glutamic acid decarboxylase 67 (Gad67) in the ACC. In the ACC of FABP3 KO mice, Gad67 promoter methylation and the binding of methyl-CpG binding protein 2 (MeCP2) and histone deacetylase 1 (HDAC1) to the Gad67 promoter are significantly decreased compared with those in WT mice.
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| Academic Significance and Societal Importance of the Research Achievements |
ACCは、認知・情動行動にかかわる脳領域と相互に線維連絡を持ち、刺激のトップダウンとボトムアップの処理や他の脳領域への適切な制御の割り当ての中心的役割を果たす。本研究の最大の特色は、ACCの神経回路に特異的な発現を示すFABP3が、高次脳機能に対して担っている意義に着目している点である。FABP3の高次脳機能における役割を明らかにすることは、ACCの脂質代謝異常が精神疾患につながるという新たな知見を提供できる点で独創性を有するといえる。
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