睡眠が認知機能の柔軟性および情動の調節に与える影響の解明
Project/Area Number |
14F04762
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Research Category |
Grant-in-Aid for JSPS Fellows
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Allocation Type | Single-year Grants |
Section | 外国 |
Research Field |
Environmental physiology(including physical medicine and nutritional physiology)
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Research Institution | University of Tsukuba |
Principal Investigator |
ラザルス ミハエル 筑波大学, 国際統合睡眠医科学研究機構, 准教授 (80469650)
|
Co-Investigator(Kenkyū-buntansha) |
MCEOWN KRISTOPHER 筑波大学, 国際統合睡眠医科学研究機構, 外国人特別研究員
MCEOWN Kristopher 筑波大学, 国際統合睡眠医科学研究機構, 外国人特別研究員
|
Project Period (FY) |
2014-04-25 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2016: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 2015: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2014: ¥900,000 (Direct Cost: ¥900,000)
|
Keywords | sleep / appetite / apetite |
Outline of Annual Research Achievements |
Human sleep proceeds in cycles. A greater amount of deep sleep is prevalent earlier in the night, while the proportion of REM sleep increases in the two cycles prior to natural awakening. It is not well understood what role REM sleep loss plays in affecting areas of the brain that control the desire to consume unhealthy foods. The prefrontal cortex (PFC) plays a role in judging the palatability of foods through taste, smell and texture. Moreover, persons who are obese tend to have increased activity in the PFC when exposed to high calorie foods. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25-48 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption. In other words, the medial prefrontal cortex may play a direct role in controlling our desire to consume weight promoting foods, high in sucrose content, when we are lacking sleep, especially REM sleep.
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Research Progress Status |
28年度が最終年度であるため、記入しない。
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Strategy for Future Research Activity |
28年度が最終年度であるため、記入しない。
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Report
(3 results)
Research Products
(2 results)