Document Detail


Food consumption inhibits pain-related behaviors.
MedLine Citation:
PMID:  19686166     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The function of the endogenous analgesia system under natural circumstances has been little explored. Our recent work shows that animals are significantly less responsive to noxious stimulation during slow wave sleep, micturition, and while eating than during quiet wake. The analgesia associated with eating is dependent on activity in the medullary raphe magnus, the final common brain stem region in endogenous analgesia pathways. Eating analgesia does not depend on energy-depletion due to food deprivation. Further, analgesia accompanies chow-eating even though chow has no sucrose, demonstrating that sucrose is not a necessary component of analgesia-evoking ingestates. Since raphe magnus modulates processing of innocuous as well as nociceptive information, the sensory suppression accompanying eating is likely a more general depression of the response to external stimulation. Such a phenomenon would serve animals well under natural conditions where energy-dense food is scarce but has counterproductive effects, possibly contributing to obesity, in modern human society where energy-dense food is readily available.
Authors:
Peggy Mason; H Foo
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  1170     ISSN:  1749-6632     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-08-18     Completed Date:  2009-09-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  399-402     Citation Subset:  IM    
Affiliation:
Department of Neurobiology, University of Chicago, Chicago, Illinois 60637, USA. pmason@uchicago.edu
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MeSH Terms
Descriptor/Qualifier:
Brain Stem / physiopathology
Feeding Behavior*
Humans
Pain / physiopathology*

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


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