Document Detail


Disruption of cue-potentiated feeding in mice with blocked ghrelin signaling.
MedLine Citation:
PMID:  23063723     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The peptide hormone ghrelin regulates a variety of eating behaviors. Not only does it potently increase intake of freely-available food, but it also shifts food preference toward diets rich in fat, enhances operant responding for food rewards, and induces conditioned place preference for food rewards. Here, we postulated that ghrelin also enables cue-potentiated feeding, in which eating is enhanced upon presentation of a food-conditioned stimulus. To test this hypothesis, a novel cue-potentiated feeding protocol adapted for use in mice was designed and validated, and then the effects of pharmacologic ghrelin receptor (GHSR) antagonism and GHSR transcriptional blockade (as occurs in GHSR-null mice) were assessed. Sated C57BL/6J mice indeed demonstrated cue-potentiated intake of grain-based pellets specifically upon presentation of a positive conditioned stimulus (CS+) but not a negative conditioned stimulus (CS-). Treatment with a GHSR antagonist blocked potentiated feeding in sated C57BL/6J mice in response to the CS+. In contrast, while GHSR-null mice also lacked a potentiation of feeding specifically in response to the CS+, they displayed an enhanced intake of pellets in response to both the positive and negative conditioned stimuli. The pattern of immediate early gene expression within the basolateral amygdala - a brain region previously linked to cue-potentiated feeding - paralleled the observed behavior of these mice, suggesting uncharacteristic activation of the amygdala in response to negative conditioned stimuli in GHSR-null mice as compared to wild-type littermates. Thus, although the observed disruptions in cue-potentiated feeding are different depending upon whether GHSR activity or GHSR expression is blocked, a key role for GHSRs in establishing a specific positive cue-food association has now been established.
Authors:
Angela K Walker; Imikomobong E Ibia; Jeffrey M Zigman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-10-09
Journal Detail:
Title:  Physiology & behavior     Volume:  108     ISSN:  1873-507X     ISO Abbreviation:  Physiol. Behav.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-03     Completed Date:  2013-05-10     Revised Date:  2014-01-10    
Medline Journal Info:
Nlm Unique ID:  0151504     Medline TA:  Physiol Behav     Country:  United States    
Other Details:
Languages:  eng     Pagination:  34-43     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Amygdala / drug effects,  metabolism
Analysis of Variance
Animals
Carrier Proteins / genetics,  metabolism
Conditioning, Operant / physiology*
Cues*
Cyclophilins / genetics,  metabolism
Cytoskeletal Proteins / genetics,  metabolism
Discrimination (Psychology) / drug effects,  physiology
Eating / drug effects,  genetics
Feeding Behavior / drug effects,  physiology*
Food Deprivation
Gene Expression Regulation / drug effects,  genetics
Ghrelin / metabolism*
Indazoles / pharmacology
Mice
Mice, Inbred C57BL
Mice, Knockout
Nerve Tissue Proteins / genetics,  metabolism
Nitrofurans / pharmacology
Proto-Oncogene Proteins c-fos / genetics,  metabolism
RNA, Messenger / metabolism
Receptors, Ghrelin / antagonists & inhibitors,  deficiency
Signal Transduction / drug effects,  genetics*
Grant Support
ID/Acronym/Agency:
1R01DA024680/DA/NIDA NIH HHS; R01 DA024680/DA/NIDA NIH HHS; T32 DA007290/DA/NIDA NIH HHS; T32DA7290/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/3-(5-nitrofuryl)-7-(5-nitrofurfurylidene)-3,3a,4,5,6,7-hexahydro-2H-indazole; 0/Carrier Proteins; 0/Cytoskeletal Proteins; 0/Ghrelin; 0/Homer protein; 0/Indazoles; 0/Nerve Tissue Proteins; 0/Nitrofurans; 0/Proto-Oncogene Proteins c-fos; 0/RNA, Messenger; 0/Receptors, Ghrelin; 0/activity regulated cytoskeletal-associated protein; EC 5.2.1.-/Cyclophilins
Comments/Corrections

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