Journal
ELIFE
Volume 9, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.54530
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Funding
- National Institutes of Health [T32-GM00832, R00 DK-97141, 1DP2DK-113750]
- Brain and Behavior Research Foundation NARSAD Young Investigator
- Esther A. and Joseph Klingenstein Fund
- Rita Allen Foundation
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From humans to vinegar flies, exposure to diets rich in sugar and fat lowers taste sensation, changes food choices, and promotes feeding. However, how these peripheral alterations influence eating is unknown. Here we used the genetically tractable organism D. melanogaster to define the neural mechanisms through which this occurs. We characterized a population of protocerebral anterior medial dopaminergic neurons (PAM DANs) that innervates the beta'2 compartment of the mushroom body and responds to sweet taste. In animals fed a high sugar diet, the response of PAM-beta'2 to sweet stimuli was reduced and delayed, and sensitive to the strength of the signal transmission out of the sensory neurons. We found that PAM-beta'2 DANs activity controls feeding rate and satiation: closed-loop optogenetic activation of beta'2 DANs restored normal eating in animals fed high sucrose. These data argue that diet-dependent alterations in taste weaken satiation by impairing the central processing of sensory signals.
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