| Project/Area Number |
16K08284
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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 |
Pharmacology in pharmacy
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| Research Institution | Kyoto Pharmaceutical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
西田 健太朗 京都薬科大学, 薬学部, 講師 (20533805)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | P2X7受容体 / アストロサイト / 酸化ストレス / 亜鉛 / うつ病 / 亜鉛トランスポータ |
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| Outline of Final Research Achievements |
In this research project, we examined whether alteration of astrocyte functionality which plays important roles in development of depressive disease was resulted from altered signaling mediated by P2X7 receptor, an ATP receptor, and zinc, and mechanism underlying taste disorder developed in depression-model mice. We have demonstrated that oxidative stress, a causative factor for depressive disease, -induced astrocyte functionality was due, at least in part, to decreased functional expression induced by alteration in intracellular zinc signaling. In addition, it appears that decreased sweet taste sensitivity in depression model mice is caused by increased expression of sweet taste receptors in circumvallate papillae in their taste buds, and 16S rRNA metagenome analyses reveal compositional change in their gut flora.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究課題の遂行によって、うつ病モデルマウスにおける亜鉛・P2X7受容体を介したアストロサイトの機能変動機構及び味覚異常分子機構を解明すると共に、脳－腸連関不全における腸内細菌叢役割を解明するための研究基盤が形成できた。これら成果は、うつ病に対する革新的治療法開発のための分子基盤の構築に加えて、味覚障害に起因した栄養素バランスの破綻及び腸内細菌叢の変動の是正が、こころの健康の維持・増進に繋がるという“食育”に繋がる重要な科学的根拠を提示できることから、極めて大きな社会貢献が期待される。
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