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

Postprandial sleep mechanics in Drosophila.

Author information

1
Department of Metabolism and Aging, The Scripps Research Institute, Jupiter, United States.
2
Program in Integrative Biology and Neuroscience, Florida Atlantic University, Jupiter, United States.
3
Department of Neuroscience, The Scripps Research Institute, Jupiter, United States.
4
Radcliffe Institute for Advanced Study, Harvard University, Cambridge, United States.
5
JP Scott Center for Neuroscience, Mind and Behavior, Bowling Green State University, Bowling Green, United States.

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.

KEYWORDS:

D. melanogaster; behavior; feeding; neurogenetics; neuroscience; nutrition; sleep

PMID:
27873574
PMCID:
PMC5119887
DOI:
10.7554/eLife.19334
[Indexed for MEDLINE]
Free PMC Article

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