Document Detail


Antagonism of sigma-1 receptors blocks compulsive-like eating.
MedLine Citation:
PMID:  22713906     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Binge eating disorder is an addiction-like disorder characterized by episodes of rapid and excessive food consumption within discrete periods of time which occur compulsively despite negative consequences. This study was aimed at determining whether antagonism of Sigma-1 receptors (Sig-1Rs) blocked compulsive-like binge eating. We trained male wistar rats to obtain a sugary, highly palatable diet (Palatable group) or a regular chow diet (Chow control group), for 1 h a day under fixed ratio 1 operant conditioning. Following intake stabilization, we evaluated the effects of the selective Sig-1R antagonist BD-1063 on food responding. Using a light/dark conflict test, we also tested whether BD-1063 could block the time spent and the food eaten in an aversive, open compartment, where the palatable diet was offered. Furthermore, we measured Sig-1R mRNA and protein expression in several brain areas of the two groups, 24 h after the last binge session. Palatable rats rapidly developed binge-like eating, escalating the 1 h intake by four times, and doubling the eating rate and the regularity of food responding, compared to Chow rats. BD-1063 dose-dependently reduced binge-like eating and the regularity of food responding, and blocked the increased eating rate in Palatable rats. In the light/dark conflict test, BD-1063 antagonized the increased time spent in the aversive compartment and the increased intake of the palatable diet, without affecting motor activity. Finally, Palatable rats showed reduced Sig-1R mRNA expression in prefrontal and anterior cingulate cortices, and a two-fold increase in Sig-1R protein expression in anterior cingulate cortex compared to control Chow rats. These findings suggest that the Sig-1R system may contribute to the neurobiological adaptations driving compulsive-like eating, opening new avenues of investigation towards pharmacologically treating binge eating disorder.
Authors:
Pietro Cottone; Xiaofan Wang; Jin Won Park; Marta Valenza; Angelo Blasio; Jina Kwak; Malliga R Iyer; Luca Steardo; Kenner C Rice; Teruo Hayashi; Valentina Sabino
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-20
Journal Detail:
Title:  Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology     Volume:  37     ISSN:  1740-634X     ISO Abbreviation:  Neuropsychopharmacology     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-16     Completed Date:  2013-03-22     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  8904907     Medline TA:  Neuropsychopharmacology     Country:  England    
Other Details:
Languages:  eng     Pagination:  2593-604     Citation Subset:  IM    
Affiliation:
Laboratory of Addictive Disorders, Departments of Pharmacology and Psychiatry, Boston University School of Medicine, Boston, MA, USA. cottone@bu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Binge-Eating Disorder / drug therapy*
Blotting, Western
Conditioning, Operant / drug effects
Dose-Response Relationship, Drug
Emotions
Male
Motivation
Motor Activity / drug effects
Piperazines / therapeutic use*
RNA, Messenger / biosynthesis,  genetics
RNA, Small Interfering / genetics
Rats
Rats, Wistar
Real-Time Polymerase Chain Reaction
Receptors, sigma / antagonists & inhibitors*,  genetics
Risk-Taking
Grant Support
ID/Acronym/Agency:
AA016731/AA/NIAAA NIH HHS; DA023680/DA/NIDA NIH HHS; DA030425/DA/NIDA NIH HHS; MH091945/MH/NIMH NIH HHS; MH093650A1/MH/NIMH NIH HHS; R00 AA016731/AA/NIAAA NIH HHS; R00 DA023680/DA/NIDA NIH HHS; R01 DA030425/DA/NIDA NIH HHS; R01 MH091945/MH/NIMH NIH HHS; R01 MH093650/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/1-(2-(3,4-dichlorophenyl)ethyl)-4-methylpiperazine; 0/Piperazines; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Receptors, sigma; 0/sigma-1 receptor
Comments/Corrections

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


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