Document Detail


Regulatory interactions of stress and reward on rat forebrain opioidergic and GABAergic circuitry.
MedLine Citation:
PMID:  21291318     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Palatable food intake reduces stress responses, suggesting that individuals may consume such ?comfort? food as self-medication for stress relief. The mechanism by which palatable foods provide stress relief is not known, but likely lies at the intersection of forebrain reward and stress regulatory circuits. Forebrain opioidergic and gamma-aminobutyric acid ergic signaling is critical for both reward and stress regulation, suggesting that these systems are prime candidates for mediating stress relief by palatable foods. Thus, the present study (1) determines how palatable ?comfort? food alters stress-induced changes in the mRNA expression of inhibitory neurotransmitters in reward and stress neurocircuitry and (2) identifies candidate brain regions that may underlie comfort food-mediated stress reduction. We used a model of palatable ?snacking? in combination with a model of chronic variable stress followed by in situ hybridization to determine forebrain levels of pro-opioid and glutamic acid decarboxylase (GAD) mRNA. The data identify regions within the extended amygdala, striatum, and hypothalamus as potential regions for mediating hypothalamic-pituitary-adrenal axis buffering following palatable snacking. Specifically, palatable snacking alone decreased pro-enkephalin-A (ENK) mRNA expression in the anterior bed nucleus of the stria terminalis (BST) and the nucleus accumbens, and decreased GAD65 mRNA in the posterior BST. Chronic stress alone increased ENK mRNA in the hypothalamus, nucleus accumbens, amygdala, and hippocampus; increased dynorphin mRNA in the nucleus accumbens; increased GAD65 mRNA in the anterior hypothalamus and BST; and decreased GAD65 mRNA in the dorsal hypothalamus. Importantly, palatable food intake prevented stress-induced gene expression changes in subregions of the hypothalamus, BST, and nucleus accumbens. Overall, these data suggest that complex interactions exist between brain reward and stress pathways and that palatable snacking can mitigate many of the neurochemical alterations induced by chronic stress.
Authors:
A M Christiansen; J P Herman; Y M Ulrich-Lai
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Stress (Amsterdam, Netherlands)     Volume:  14     ISSN:  1607-8888     ISO Abbreviation:  Stress     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-04     Completed Date:  2011-05-16     Revised Date:  2014-09-13    
Medline Journal Info:
Nlm Unique ID:  9617529     Medline TA:  Stress     Country:  England    
Other Details:
Languages:  eng     Pagination:  205-15     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Enkephalins / biosynthesis*,  genetics
Glutamate Decarboxylase / biosynthesis*
Male
Prosencephalon / metabolism*
Protein Precursors / biosynthesis*,  genetics
RNA, Messenger / metabolism
Rats
Rats, Long-Evans
Reward*
Septal Nuclei / metabolism
Stress, Psychological / physiopathology*
Grant Support
ID/Acronym/Agency:
DK059803/DK/NIDDK NIH HHS; DK067820/DK/NIDDK NIH HHS; DK078906/DK/NIDDK NIH HHS; F32 DK067820/DK/NIDDK NIH HHS; F32 DK067820-02/DK/NIDDK NIH HHS; K01 DK078906/DK/NIDDK NIH HHS; K01 DK078906-01/DK/NIDDK NIH HHS; K01 DK078906-02/DK/NIDDK NIH HHS; K01 DK078906-03/DK/NIDDK NIH HHS; K01 DK078906-04/DK/NIDDK NIH HHS; MH049698/MH/NIMH NIH HHS; MH069725/MH/NIMH NIH HHS; R01 MH049698/MH/NIMH NIH HHS; R01 MH049698-14/MH/NIMH NIH HHS; R01 MH049698-15/MH/NIMH NIH HHS; R01 MH049698-17/MH/NIMH NIH HHS; R01 MH049698-20/MH/NIMH NIH HHS; R01 MH069725/MH/NIMH NIH HHS; R01 MH069725-04/MH/NIMH NIH HHS; R01 MH069725-05/MH/NIMH NIH HHS; T32 DK059803-07/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Enkephalins; 0/Protein Precursors; 0/RNA, Messenger; 0/proenkephalin; EC 4.1.1.15/Glutamate Decarboxylase; EC 4.1.1.15/glutamate decarboxylase 2
Comments/Corrections

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