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Central Amygdala Prepronociceptin-Expressing Neurons Mediate Palatable Food Consumption and Reward.
- Source :
-
Neuron [Neuron] 2019 Jun 05; Vol. 102 (5), pp. 1037-1052.e7. Date of Electronic Publication: 2019 Apr 24. - Publication Year :
- 2019
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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 (Pnoc <superscript>CeA</superscript> ) that are activated by palatable food consumption. Ablation or chemogenetic inhibition of these cells reduces palatable food consumption. Additionally, ablation of Pnoc <superscript>CeA</superscript> cells reduces high-fat-diet-driven increases in bodyweight and adiposity. Pnoc <superscript>CeA</superscript> 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 Pnoc <superscript>CeA</superscript> 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.<br /> (Copyright © 2019 Elsevier Inc. All rights reserved.)
- Subjects :
- Adiposity
Animals
Body Weight
Central Amygdaloid Nucleus physiology
Diet, High-Fat
Mice
Neural Pathways
Neurons physiology
Parabrachial Nucleus metabolism
Parabrachial Nucleus physiology
Patch-Clamp Techniques
Protein Precursors genetics
Receptors, Opioid genetics
Septal Nuclei metabolism
Septal Nuclei physiology
Solitary Nucleus metabolism
Solitary Nucleus physiology
Central Amygdaloid Nucleus metabolism
Feeding Behavior physiology
Neurons metabolism
Protein Precursors metabolism
Receptors, Opioid metabolism
Reward
Subjects
Details
- Language :
- English
- ISSN :
- 1097-4199
- Volume :
- 102
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Neuron
- Publication Type :
- Academic Journal
- Accession number :
- 31029403
- Full Text :
- https://doi.org/10.1016/j.neuron.2019.03.037