Document Detail


Reduction of food intake by cholecystokinin requires activation of hindbrain NMDA-type glutamate receptors.
MedLine Citation:
PMID:  21562094     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intraperitoneal injection of CCK reduces food intake and triggers a behavioral pattern similar to natural satiation. Reduction of food intake by CCK is mediated by vagal afferents that innervate the stomach and small intestine. These afferents synapse in the hindbrain nucleus of the solitary tract (NTS) where gastrointestinal satiation signals are processed. Previously, we demonstrated that intraperitoneal (IP) administration of either competitive or noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists attenuates reduction of food intake by CCK. However, because vagal afferents themselves express NMDA receptors at both central and peripheral endings, our results did not speak to the question of whether NMDA receptors in the brain play an essential role in reduction of feeding by CCK. We hypothesized that activation of NMDA receptors in the NTS is necessary for reduction of food intake by CCK. To test this hypothesis, we measured food intake following IP CCK, subsequent to NMDA receptor antagonist injections into the fourth ventricle, directly into the NTS or subcutaneously. We found that either fourth-ventricle or NTS injection of the noncompetitive NMDA receptor antagonist MK-801 was sufficient to inhibit CCK-induced reduction of feeding, while the same antagonist doses injected subcutaneously did not. Similarly fourth ventricle injection of d-3-(2-carboxypiperazin-4-yl)-1-propenyl-1-phosphoric acid (d-CPPene), a competitive NMDA receptor antagonist, also blocked reduction of food intake following IP CCK. Finally, d-CPPene injected into the fourth ventricle attenuated CCK-induced expression of nuclear c-Fos immunoreactivity in the dorsal vagal complex. We conclude that activation of NMDA receptors in the hindbrain is necessary for the reduction of food intake by CCK. Hindbrain NMDA receptors could comprise a critical avenue for control and modulation of satiation signals to influence food intake and energy balance.
Authors:
Jason Wright; Carlos Campos; Thiebaut Herzog; Mihai Covasa; Krzysztof Czaja; Robert C Ritter
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-05-11
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  301     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-08-03     Completed Date:  2011-10-18     Revised Date:  2014-09-13    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R448-55     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cholecystokinin / pharmacology*
Dizocilpine Maleate / administration & dosage,  pharmacology
Eating / drug effects*
Gene Expression Regulation / physiology
Genes, fos / physiology
Injections, Intraventricular
Male
Piperazines / administration & dosage,  pharmacology
Rats
Rats, Sprague-Dawley
Receptors, Glutamate / classification,  metabolism*
Rhombencephalon / drug effects*,  physiology
Satiation
Grant Support
ID/Acronym/Agency:
DK-52849/DK/NIDDK NIH HHS; NS-20561/NS/NINDS NIH HHS; R01 DK052849/DK/NIDDK NIH HHS; R01 NS020561/NS/NINDS NIH HHS; R01 NS020561-27/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Piperazines; 0/Receptors, Glutamate; 137424-80-7/SDZ EAA 494; 6LR8C1B66Q/Dizocilpine Maleate; 9011-97-6/Cholecystokinin
Comments/Corrections

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


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