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

Abstract

SummaryThe motivation to eat is suppressed by satiety and by aversive stimuli such as nausea. Compared to the neural regulation of homeostatic feeding, the mechanism of appetite suppression by nausea is not well understood. Previous work characterized PKCδ neurons in the lateral subdivision (CeL) of the central amygdala (CeA) to suppress feeding in response to satiety signals and nausea. Here, we characterized a previously unknown neuronal population enriched in the medial subdivision (CeM) of the CeA and marked by expression of Dlk1. Distinct from CeAPKCδneurons, CeADlk1neurons are activated by nausea, but not by satiety, form long-range projections to many brain regions and exert their anorexigenic activity by inhibition of neurons of the parabrachial nucleus. CeADlk1neurons are under inhibitory control of appetitive CeA neurons, but also receive long-range monosynaptic inputs from multiple brain regions. Our results illustrate a novel CeA circuit that regulates nausea-induced feeding suppression.HighlightsCeADlk1neurons are a previously unknown CeA cell population, enriched in the CeMCeADlk1neurons are activated by nausea and bitter food, but not satietyCeADlk1neurons suppress feeding under conditions of nauseaCeADlk1neuronal projections to the PBN mediate feeding suppression