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进食后睡眠力学在.

Postprandial sleep mechanics in .

机构信息

Department of Metabolism and Aging, The Scripps Research Institute, Jupiter, United States.

Program in Integrative Biology and Neuroscience, Florida Atlantic University, Jupiter, United States.

出版信息

Elife. 2016 Nov 22;5:e19334. doi: 10.7554/eLife.19334.

Abstract

Food consumption is thought to induce sleepiness. However, little is known about how postprandial sleep is regulated. Here, we simultaneously measured sleep and food intake of individual flies and found a transient rise in sleep following meals. Depending on the amount consumed, the effect ranged from slightly arousing to strongly sleep inducing. Postprandial sleep was positively correlated with ingested volume, protein, and salt-but not sucrose-revealing meal property-specific regulation. Silencing of leucokinin receptor (Lkr) neurons specifically reduced sleep induced by protein consumption. Thermogenetic stimulation of leucokinin (Lk) neurons decreased whereas Lk downregulation by RNAi increased postprandial sleep, suggestive of an inhibitory connection in the Lk-Lkr circuit. We further identified a subset of non-leucokininergic cells proximal to Lkr neurons that rhythmically increased postprandial sleep when silenced, suggesting that these cells are cyclically gated inhibitory inputs to Lkr neurons. Together, these findings reveal the dynamic nature of postprandial sleep.

摘要

人们认为食物的摄入会引起困意。然而,人们对于进食后如何调节睡眠知之甚少。在这里,我们同时测量了个体果蝇的睡眠和进食情况,发现进食后睡眠会出现短暂的增加。根据摄入的量,这种影响的范围从轻微唤醒到强烈诱导睡眠。进食后睡眠与摄入的量、蛋白质和盐呈正相关,但与蔗糖无关,这表明存在特定于膳食特性的调节。沉默白细胞激肽受体 (Lkr) 神经元特异性减少了由蛋白质摄入引起的睡眠。热原刺激白细胞激肽 (Lk) 神经元会减少,而 RNAi 下调 Lk 会增加进食后的睡眠,这表明在 Lk-Lkr 回路中存在抑制性连接。我们进一步鉴定出一组靠近 Lkr 神经元的非白细胞激肽能细胞,当它们被沉默时会周期性地增加进食后的睡眠,这表明这些细胞是 Lkr 神经元的周期性门控抑制性输入。总的来说,这些发现揭示了进食后睡眠的动态性质。

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