2014 Fiscal Year Annual Research Report
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 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)
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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
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Project Period (FY) |
2014-04-25 – 2017-03-31
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Keywords | sleep / apetite |
Outline of Annual Research Achievements |
Data is beginning to emerge which links specific brain function with insufficient sleep and the desire to consume weight promoting/highly palatable foods. When healthy adults are acutely deprived of sleep for more than 24 hours the effects on brain function are dramatic. Specifically, recent findings in sleep deprived persons found reduced fMRI activation in areas of the brain that mediate decision making (e.g., the prefrontal cortex) while at the same time increasing activation in centers of the brain that mediate emotion (e.g., the amygdala) when subsequently exposed to pictures of high calorie foods (Greer S, et al., Nat Commun 2013, 2259). Our lab discovered that caffeine facilitates consumption of a high sucrose diet (white chocolate) and decreases consumption of regular diet (McEown K, et al., unpublished data), however it remains unclear if this is due to prolonged wakefulness or other caffeine effects such as increased anxiety.
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Current Status of Research Progress |
Current Status of Research Progress
1: Research has progressed more than it was originally planned.
Reason
We are now developing an insomnia mouse model to examine the effect of sleep restriction on appetite for highly palatable foods and investigate the interacting roles that the amygdala, prefrontal cortex and nucleus accumbens shell play in mediating appetite after sleep restriction.
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Strategy for Future Research Activity |
Inducing sleep restriction via nucleus accumbens shell inactivation will be compared to other sleep restriction methods to examine the efficacy of each method on appetite for highly palatable foods. Firstly, caffeine will be used as a comparison method to restrict sleep in mice. Paterson et al. (see Paterson L, et al., J Psychopharmacol 2009, 23) observed that systematic caffeine injections at a 30mg/kg significantly facilitates wakefulness over a six hour period from 33% wake time in vehicle injected controls to 69% wake time in caffeine injected animals. Secondly, a mechanical sleep deprivation device will be developed that provides physical stimulation to induce sleep restriction. The device consists of a Plexiglas chamber in which mice are placed in groupings of five. A camera mounted above the chamber tracks movement of all animals within the chamber. When an animal ceases movement for more than one minute, a computer program activates a shaking movement of the entire chamber which awakens the animal. This device will be used to restrict sleep for a period of 6 hours out of every 24 hour period for four days to match sleep restriction produced from caffeine injections and nucleus accumbens shell IVM-GluClαβ mediated inactivation.
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