Document Detail


Reversible suppression of food reward behavior by chronic mu-opioid receptor antagonism in the nucleus accumbens.
MedLine Citation:
PMID:  20654704     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Overindulgence in easily available energy-dense palatable foods is thought to be an important factor in the current obesity epidemic but the underlying neural mechanisms are not well understood. Here we demonstrate that mu-opioid receptor signaling in the nucleus accumbens may be important. Protracted suppression of endogenous mu-opioid receptor signaling focused on the nucleus accumbens shell for several days by means of microinjected beta-funaltrexamine (BFNA) diminished both "liking" of sucrose, as indicated by fewer positive hedonic orofacial responses, and the incentive reinforcement value ("wanting") of a food reward, as indicated by lower completion speed and increased time being distracted in the incentive runway. BFNA-treatment also decreased responding to sucrose and corn oil in the brief access lick paradigm, a test measuring a combination of mainly taste-guided "liking" and low-effort "wanting", as well as 4 h intake of sucrose solution. These effects were not due to nonspecific permanent neuronal changes, as they were fully reversible. We conclude that endogenous mu-opioid signaling in the nucleus accumbens is necessary for the full display of palatable food-induced hyperphagia through mechanisms including hedonic, motivational, and reinforcement processes. Development of obesity could be the result of predisposing innate differences in these mechanisms or overstimulation of these mechanisms by external factors.
Authors:
A C Shin; P J Pistell; C B Phifer; H R Berthoud
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-07-27
Journal Detail:
Title:  Neuroscience     Volume:  170     ISSN:  1873-7544     ISO Abbreviation:  Neuroscience     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-03     Completed Date:  2011-01-20     Revised Date:  2011-10-13    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  580-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
Affiliation:
Neurobiology of Nutrition Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Appetitive Behavior / physiology*
Male
Microinjections
Motivation / physiology
Naltrexone / administration & dosage,  analogs & derivatives*,  pharmacology
Nucleus Accumbens / drug effects,  physiology*
Rats
Rats, Sprague-Dawley
Receptors, Opioid, mu / antagonists & inhibitors,  physiology*
Reinforcement (Psychology)
Reward
Sucrose
Grant Support
ID/Acronym/Agency:
DK047348/DK/NIDDK NIH HHS; DK071082/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Opioid, mu; 16590-41-3/Naltrexone; 57-50-1/Sucrose; 72782-05-9/beta-funaltrexamine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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