Postprandial sleep mechanics in Drosophila

eLife

Maria E Yurgel¹  Sonali A Deshpande²  Keith R Murphy³  Ken Dawson-Scully³  Alex C Keene³  James P Quinn³  Seth M Tomchik⁴  Jennifer L Weissbach⁴  Robert Huber⁴  William W Ja⁵ 

[1] Department of Neuroscience, The Scripps Research Institute, Jupiter, United States;Program in Integrative Biology and Neuroscience, Florida Atlantic University, Jupiter, United States;Department of Metabolism and Aging, The Scripps Research Institute, Jupiter, United States;Program in Integrative Biology and Neuroscience, Florida Atlantic University, Jupiter, United States;Radcliffe Institute for Advanced Study, Harvard University, Cambridge, United States;

关键词: feeding;    sleep;    behavior;    neurogenetics;    nutrition;   

DOI  :  10.7554/eLife.19334

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown