The neural mechanism regulating acute moderate exercise-induced enhancement of long-term memory
| Project/Area Number |
26750307
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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 |
Sports science
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| Research Institution | Health Sciences University of Hokkaido |
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Principal Investigator |
INOUE Koshiro 北海道医療大学, リハビリテーション科学部, 講師 (30708574)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 一過性中強度運動 / 記憶の固定化 / 海馬CA1 / タンパク質合成 / 扁桃体 / 記憶固定化 / 位置認識試験 / 新規タンパク質 / 逆行性トレーサー / 長期記憶 / 海馬 / 新規タンパク質合成 / 乳酸性作業閾値 / SDラット |
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| Outline of Final Research Achievements |
Long-term memory consolidation requires de novo protein synthesis in hippocampal CA1 region, and the protein synthesis-dependent memory consolidation is partially controlled by amygdala activation. In this study, we examined whether acute moderate exercise (AME) boosts memory consolidation via newly protein synthesis in the hippocampal CA1, and whether the effects are shaped by input from amygdala. Our results, in rats, demonstrated that post-learning AME enhances memory consolidation, resulting in improved long-term memory, and that the AME-induced memory consolidation is abolished with protein synthesis inhibitor treatment in the hippocampal CA1. The findings partially support our hypothesis, but further studies are necessary to test whether the activation of amygdala-hippocampus circuit by AME could contribute to the AME-induced memory consolidation.
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Report
(4 results)
Research Products
(5 results)
