| Project/Area Number |
17K08117
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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 |
Veterinary medical science
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| Research Institution | Azabu University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | AChE / ChAT / ACh / グリア細胞 |
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| Outline of Final Research Achievements |
This study focused on the expression and regulation function of acetylcholine (ACh) -related enzymes, especially ACh esterase (AChE), in activation of glial cells. In the injury area in cerebral cortex of a mouse TBI model, increase of AChE- and choline acetyltransferase (ChAT)-immunopositive signals was immunohistochemically detected in reactive glial cells, and ACh amount was also increased. Reactive state of primary cultured astrocytes wasn’t affected by treatment with AChE inhibitor. Contrary to our expectation that AChE inhibitor administration decreases the size of the injured area in the cerebral cortex of the model, the inhibitor increased the size and the immunopositive signals of reactive-microglial marker in the injured area, and didn’t that of astrocytes. Therefore, AChE increased by TBI seems to have regulatory function on reaction state of microglia.
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| Academic Significance and Societal Importance of the Research Achievements |
中枢神経系には，神経機能の主体である神経細胞とそれをサポートするグリア細胞が存在する。脳が傷害されると修復のためにグリア細胞が活性化されるが，過剰な活性化は神経細胞死を引き起こし予後を悪くする。神経膠細胞の活性化制御により，この増悪を抑制する可能性がある。本研究ではAChとACh関連酵素とグリア細胞の中でもアストロサイトとマイクログリアの関連を検討し検討を行った。マイクログリア活性化にAChEが関与する可能性が示されたことは，今後は詳細な検討が必要ではあるが，脳障害時の予後改善に関わる一要因としての情報となるであろう。
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