Nausea-induced suppression of feeding is mediated by central amygdala Dlk1-expressing neurons

The motivation to eat is suppressed by satiety and aversive stimuli such as nausea. The neural circuit mechanisms of appetite suppression by nausea are not well understood. Pkcδ neurons in the lateral subdivision of the central amygdala (CeA) suppress feeding in response to satiety signals and nausea. Here, we characterized neurons enriched in the medial subdivision (CeM) of the CeA marked by expression of Dlk1. CeADlk1 neurons are activated by nausea, but not satiety, and specifically suppress feeding induced by nausea. Artificial activation of CeADlk1 neurons suppresses drinking and social interactions, suggesting a broader function in attenuating motivational behavior. CeADlk1 neurons form projections to many brain regions and exert their anorexigenic activity by inhibition of neurons of the parabrachial nucleus. CeADlk1 neurons are inhibited by appetitive CeA neurons, but also receive long-range monosynaptic inputs from multiple brain regions. Our results illustrate a CeA circuit that regulates nausea-induced feeding suppression. [Display omitted] •CeADlk1 neurons are activated by nausea, visceral malaise, and bitter liquid, but not satiety•CeADlk1 neurons suppress feeding under conditions of nausea•Artificial activation of CeADlk1 neurons inhibits ongoing consummatory behavior•CeADlk1 neuronal projections to the PBN mediate feeding suppression Ding et al. characterize a neuron population in central amygdala that is activated by nausea and suppresses feeding under conditions of nausea by inhibiting neurons in the parabrachial nucleus.