Dataset Information

Central Amygdala Prepronociceptin-Expressing Neurons Mediate Palatable Food Consumption and Reward.

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.

SUBMITTER: Hardaway JA

PROVIDER: S-EPMC6750705 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Central Amygdala Prepronociceptin-Expressing Neurons Mediate Palatable Food Consumption and Reward.

Hardaway J Andrew JA Halladay Lindsay R LR Mazzone Christopher M CM Pati Dipanwita D Bloodgood Daniel W DW Kim Michelle M Jensen Jennifer J DiBerto Jeffrey F JF Boyt Kristen M KM Shiddapur Ami A Erfani Ava A Hon Olivia J OJ Neira Sofia S Stanhope Christina M CM Sugam Jonathan A JA Saddoris Michael P MP Tipton Greg G McElligott Zoe Z Jhou Thomas C TC Stuber Garret D GD Bruchas Michael R MR Bulik Cynthia M CM Holmes Andrew A Kash Thomas L TL

Neuron 20190424 5

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<sup>CeA</sup>) that are activated by palatable food consumption. Ablation or chemogenetic inhibition of these cells reduces palatable food consumption. Additionally, ablation of Pnoc<sup>CeA</sup> cells reduces high-fat-diet-driven increase ...[more]

PMID: 31029403

Similar Datasets

Project description:Background/objectivesDysfunction in reward-related aspects of feeding, and consequent overeating in humans, is a major contributor to obesity. Intrauterine undernutrition and overnutrition are among the predisposing factors, but the exact mechanism of how overeating develops is still unclear. Consummatory behavior is regulated by the medial shell (mSh) of the accumbens nucleus (Nac) through direct connections with the rostral part of the lateral hypothalamic area (LHA). Our aim was to investigate whether an altered Nac-LHA circuit may underlie hyperphagic behavior.Subjects/methodsIntrauterine protein-restricted (PR) male Wistar rats were used as models for hyperphagia. The experiments were performed using young adult control (normally nourished) and PR animals. Sweet condensed milk (SCM) served as a reward to test consumption and subsequent activation (Fos+) of Nac and LHA neurons. Expression levels of type 1 and 2 dopamine receptors (D1R, D2R) in the Nac, as well as tyrosine hydroxylase (TH) levels in the ventral tegmental area, were determined. The D1R agonist SKF82958 was injected into the mSh-Nac of control rats to test the effect of D1R signaling on SCM intake and neuronal cell activation in the LHA.ResultsA group of food reward-representing D1R+ neurons was identified in the mSh-Nac. Activation (Fos+) of these neurons was highly proportional to the consumed palatable food. D1R agonist treatment attenuated SCM intake and diminished the number of SCM-activated cells in the LHA. Hyperphagic PR rats showed increased intake of SCM, reduced D1R expression, and an impaired response to SCM-evoked neuronal activation in the mSh-Nac, accompanied by an elevated number of Fos+ neurons in the LHA compared to controls.ConclusionsSensitivity of food reward-representing neurons in the mSh-Nac determines the level of satisfaction that governs cessation of consumption, probably through connections with the LHA. D1R signaling is a key element in this function, and is impaired in obesity-prone rats.

Dataset Information

Central Amygdala Prepronociceptin-Expressing Neurons Mediate Palatable Food Consumption and Reward.

Publications

Central Amygdala Prepronociceptin-Expressing Neurons Mediate Palatable Food Consumption and Reward.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets