| Literature DB >> 31029403 |
J Andrew Hardaway1, Lindsay R Halladay2, Christopher M Mazzone3, Dipanwita Pati4, Daniel W Bloodgood3, Michelle Kim4, Jennifer Jensen4, Jeffrey F DiBerto4, Kristen M Boyt4, Ami Shiddapur4, Ava Erfani4, Olivia J Hon3, Sofia Neira3, Christina M Stanhope4, Jonathan A Sugam4, Michael P Saddoris5, Greg Tipton4, Zoe McElligott6, Thomas C Jhou7, Garret D Stuber8, Michael R Bruchas9, Cynthia M Bulik10, Andrew Holmes11, Thomas L Kash12.
Abstract
Food palatability is one of many factors that drives food consumption, and the hedonic drive to feed is a key contributor to obesity and binge eating. In this study, we identified a population of prepronociceptin-expressing cells in the central amygdala (PnocCeA) that are activated by palatable food consumption. Ablation or chemogenetic inhibition of these cells reduces palatable food consumption. Additionally, ablation of PnocCeA cells reduces high-fat-diet-driven increases in bodyweight and adiposity. PnocCeA neurons project to the ventral bed nucleus of the stria terminalis (vBNST), parabrachial nucleus (PBN), and nucleus of the solitary tract (NTS), and activation of cell bodies in the central amygdala (CeA) or axons in the vBNST, PBN, and NTS produces reward behavior but did not promote feeding of palatable food. These data suggest that the PnocCeA network is necessary for promoting the reinforcing and rewarding properties of palatable food, but activation of this network itself is not sufficient to promote feeding.Entities:
Keywords: binge eating; central amygdala; nociceptin; nucleus of the solitary tract; obesity; parabrachial nucleus; reward
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Year: 2019 PMID： 31029403 PMCID： PMC6750705 DOI： 10.1016/j.neuron.2019.03.037
Source DB: PubMed Journal: Neuron ISSN： 0896-6273 Impact factor: 17.173