2015 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 |
We developed a novel mechanical device with the intention of producing sleep loss in mice over a 72-hour period. The SRD was a wire-mesh-grid device placed in the bottom of the housing cage. EEG/EMG recordings indicated that the SRD significantly reduced rapid-eye movement (REM) sleep during the dark period at 24-48-hours (p<.05) and 48-72-hours after device introduction. In addition, the SRD increased wakefulness during the dark period 48-72-hours after device introduction (p<.05). We then tested the effect of the SRD on stress and fear responses in mice. We found that 72-hours of SRD exposure significantly increased plasma corticosterone levels compared to naïve control mice (p<.01). However, mice exposed to the SRD had significantly lower plasma corticosterone levels compared to caffeine injected mice (30 mg/kg, i.p; p<.05). Finally, SRD exposure did not effect unconditioned fear behavior in the elevated plus maze (all comparisons p>.05). These results suggest that SRD exposure produces mild stress responses, however, unconditioned fear is unaffected by SRD exposure.
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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
While we are in the process of finalizing data collection, we have started to write a paper, entitled "Medial prefrontal cortex neuronal inhibition reverses the effects of rapid eye movement sleep loss on highly palatable food consumption in mice."
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Strategy for Future Research Activity |
We will explore the interacting roles of the PFC, amygdala and NAc in modulating sleep and appetite for highly palatable foods. The IVM-GluClαβ technique will be used to specifically inhibit neuronal functioning in the NAc shell, amygdala and PFC. Sleep architecture and appetite for highly palatable foods will be measured while inactivating these brain regions. After EEG recording and food consumption measures are obtained, mice will be sacrificed and the location of AAV microinjections within the brain will be visualized using high resolution light/fluorescence microscopy via identification of fluorescent mCherry protein.
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