Document Detail


Pharmacological enhancement of the endocannabinoid system in the nucleus accumbens shell stimulates food intake and increases c-Fos expression in the hypothalamus.
MedLine Citation:
PMID:  17549045     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: Evidence indicates that the endocannabinoid, 2-arachidonoylglycerol (2-AG), increases food intake when injected into the nucleus accumbens shell (NAcS), thereby potentially activating hypothalamic nuclei involved in food intake regulation. We aimed to evaluate potential orexigenic effects of the endocannabinoid anandamide and of AA5HT, a fatty acid amide hydrolase (FAAH) inhibitor, and OMDM-1, an inhibitor of anandamide uptake, injected in the NAcS, as well as the effect of these treatments on activation of hypothalamic nuclei.
EXPERIMENTAL APPROACH: Drugs were given into the NAcS of rats and food intake quantified during the next 4 h. In other groups, after the same treatments the brains were processed for c-Fos immunohistochemistry with focus on hypothalamic nuclei. Additional groups were used to quantify endocannabinoid levels in the nucleus accumbens and the hypothalamus after AA5HT and OMDM-1 intra-NAcS injections.
KEY RESULTS: Our results indicate that the above treatments stimulate food intake during 4 h post-injection. They also increase c-Fos immunoreactivity in hypothalamic nuclei. The CB(1) antagonist, AM251, blocked these effects. Finally, we found elevated levels of 2-AG, but not anandamide, after intra-NAcS injections of AA5HT.
CONCLUSIONS AND IMPLICATIONS: These data support the involvement of the endocannabinoid system in feeding behavior at the level of the NAcS and hypothalamus. In addition, this is the first experimental demonstration that the pharmacological inhibition of endocannabinoid inactivation in the NAcS stimulates food intake, suggesting that the endocannabinoid degrading proteins can be a target for treating eating disorders.
Authors:
E Soria-Gómez; I Matias; P E Rueda-Orozco; M Cisneros; S Petrosino; L Navarro; V Di Marzo; O Prospéro-García
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-06-04
Journal Detail:
Title:  British journal of pharmacology     Volume:  151     ISSN:  0007-1188     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-07-30     Completed Date:  2007-11-02     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1109-16     Citation Subset:  IM    
Affiliation:
Grupo de Neurociencias, Depto. de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico DF 04510, Mexico.
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MeSH Terms
Descriptor/Qualifier:
Amidohydrolases / antagonists & inhibitors,  metabolism
Animals
Arachidonic Acids / metabolism,  pharmacology
Arcuate Nucleus / drug effects,  metabolism
Benzyl Compounds / pharmacology
Cannabinoid Receptor Modulators / metabolism*,  physiology
Eating / drug effects,  physiology*
Endocannabinoids*
Glycerides / metabolism
Hypothalamus / drug effects,  metabolism*
Immunohistochemistry
Male
Nucleus Accumbens / drug effects,  metabolism*
Piperidines / pharmacology
Polyunsaturated Alkamides / pharmacology
Proto-Oncogene Proteins c-fos / biosynthesis*,  metabolism
Pyrazoles / pharmacology
Rats
Rats, Wistar
Receptor, Cannabinoid, CB1 / metabolism
Serotonin / analogs & derivatives,  pharmacology
Time Factors
Chemical
Reg. No./Substance:
0/AM 251; 0/Arachidonic Acids; 0/Benzyl Compounds; 0/Cannabinoid Receptor Modulators; 0/Endocannabinoids; 0/Glycerides; 0/OMDM-1 cpd; 0/Piperidines; 0/Polyunsaturated Alkamides; 0/Proto-Oncogene Proteins c-fos; 0/Pyrazoles; 0/Receptor, Cannabinoid, CB1; 0/arachidonoylserotonin; 50-67-9/Serotonin; 53847-30-6/2-arachidonylglycerol; 94421-68-8/anandamide; EC 3.5.-/Amidohydrolases; EC 3.5.1.-/fatty-acid amide hydrolase
Comments/Corrections

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