The Neuroscience Graduate Program, The University of Michigan, Ann Arbor, United States; Department of Molecular, Cellular and Developmental Biology, College of Literature, Science, and the Arts, The University of Michigan, Ann Arbor, United States
Julia Rosander
The Undergraduate Program in Neuroscience, College of Literature, Science, and the Arts, The University of Michigan, Ann Arbor, United States
Jennifer Gottfried
The Undergraduate Program in Neuroscience, College of Literature, Science, and the Arts, The University of Michigan, Ann Arbor, United States
Evan Dennis
The Undergraduate Program in Neuroscience, College of Literature, Science, and the Arts, The University of Michigan, Ann Arbor, United States
The Neuroscience Graduate Program, The University of Michigan, Ann Arbor, United States; Department of Molecular, Cellular and Developmental Biology, College of Literature, Science, and the Arts, The University of Michigan, Ann Arbor, United States; The Undergraduate Program in Neuroscience, College of Literature, Science, and the Arts, The University of Michigan, Ann Arbor, United States
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 β’2 compartment of the mushroom body and responds to sweet taste. In animals fed a high sugar diet, the response of PAM-β’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-β’2 DANs activity controls feeding rate and satiation: closed-loop optogenetic activation of β’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.
