Author
Listed:
- Sarah Cains
(The Francis Crick Institute, Mill Hill Laboratory)
- Craig Blomeley
(The Francis Crick Institute, Mill Hill Laboratory)
- Mihaly Kollo
(Physiology and Pharmacology, University College London)
- Romeo Rácz
(The Francis Crick Institute, Mill Hill Laboratory)
- Denis Burdakov
(The Francis Crick Institute, Mill Hill Laboratory
Institute of Psychiatry, Psychology and Neuroscience, King’s College London)
Abstract
Alcohol intake associates with overeating in humans. This overeating is a clinical concern, but its causes are puzzling, because alcohol (ethanol) is a calorie-dense nutrient, and calorie intake usually suppresses brain appetite signals. The biological factors necessary for ethanol-induced overeating remain unclear, and societal causes have been proposed. Here we show that core elements of the brain’s feeding circuits—the hypothalamic Agrp neurons that are normally activated by starvation and evoke intense hunger—display electrical and biochemical hyperactivity on exposure to dietary doses of ethanol in brain slices. Furthermore, by circuit-specific chemogenetic interference in vivo, we find that the Agrp cell activity is essential for ethanol-induced overeating in the absence of societal factors, in single-housed mice. These data reveal how a widely consumed nutrient can paradoxically sustain brain starvation signals, and identify a biological factor required for appetite evoked by alcohol.
Suggested Citation
Sarah Cains & Craig Blomeley & Mihaly Kollo & Romeo Rácz & Denis Burdakov, 2017.
"Agrp neuron activity is required for alcohol-induced overeating,"
Nature Communications, Nature, vol. 8(1), pages 1-8, April.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14014
DOI: 10.1038/ncomms14014
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