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Nat Neurosci. 2017 Oct;20(10):1384-1394. doi: 10.1038/nn.4623. Epub 2017 Aug 21.

Central amygdala circuits modulate food consumption through a positive-valence mechanism.

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Molecules-Signaling-Development, Max Planck Institute of Neurobiology, Martinsried, Germany.
Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Max von Pettenkofer-Institute &Gene Center, Ludwig-Maximilians-University Munich, Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.


The complex behaviors underlying reward seeking and consumption are integral to organism survival. The hypothalamus and mesolimbic dopamine system are key mediators of these behaviors, yet regulation of appetitive and consummatory behaviors outside of these regions is poorly understood. The central nucleus of the amygdala (CeA) has been implicated in feeding and reward, but the neurons and circuit mechanisms that positively regulate these behaviors remain unclear. Here, we defined the neuronal mechanisms by which CeA neurons promote food consumption. Using in vivo activity manipulations and Ca2+ imaging in mice, we found that GABAergic serotonin receptor 2a (Htr2a)-expressing CeA neurons modulate food consumption, promote positive reinforcement and are active in vivo during eating. We demonstrated electrophysiologically, anatomically and behaviorally that intra-CeA and long-range circuit mechanisms underlie these behaviors. Finally, we showed that CeAHtr2a neurons receive inputs from feeding-relevant brain regions. Our results illustrate how defined CeA neural circuits positively regulate food consumption.

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