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

阐明睡眠对认知灵活性和情绪调节的影响

基本信息

批准号：
14F04762
负责人：
ラザルスミハエル
金额：
$ 1.47万
依托单位：
University of Tsukuba
依托单位国家：
日本
项目类别：
Grant-in-Aid for JSPS Fellows
财政年份：
2014
资助国家：
日本
起止时间：
2014-04-25 至 2017-03-31
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-14F04762/
关键词：
sleep appetite apetite

项目摘要

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.

人睡眠以周期进行。晚上早些时候普遍存在更高的睡眠，而自然觉醒之前的两个周期中，REM睡眠的比例增加。尚不清楚REM睡眠损失在影响控制食用不健康食物渴望的大脑区域的作用。前额叶皮层（PFC）在通过味道，气味和质地来判断食品的可口性方面发挥了作用。此外，肥胖的人暴露于高热量食品时，PFC的活动往往会增加。但是，尚不清楚PFC在REM睡眠剥夺后对高度可口食品（HPF）的奖励反应中的确切作用尚不清楚。我们在25-48小时的时间内有选择地降低了小鼠的REM睡眠，化学遗传性通过使用改变的谷氨酸门控和伊维菌素门控氯化物通道抑制内侧PFC（MPFC），从而通过超极化神经元促进神经元抑制。在MPFC失活并诱导REM睡眠损失时测量HPF消耗。我们发现，与对照动物相比，REM睡眠损失增加了HPF的消耗。但是，MPFC的失活反转了REM睡眠损失对蔗糖消耗的影响，而不会影响脂肪的消耗。我们的发现首次提供了REM睡眠，MPFC功能和HPF消耗之间的因果关系。换句话说，内侧前额叶皮层可能在控制我们缺乏睡眠（尤其是REM睡眠）时促进体重促进食物的渴望促进食物的渴望中发挥直接作用。