Document Detail


Convergent, not serial, striatal and pallidal circuits regulate opioid-induced food intake.
MedLine Citation:
PMID:  19336249     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mu opioid receptor (MOR) signaling in the nucleus accumbens (NAcc) elicits marked increases in the consumption of palatable tastants. However, the mechanism and circuitry underlying this effect are not fully understood. Multiple downstream target regions have been implicated in mediating this effect but the role of the ventral pallidum (VP), a primary target of NAcc efferents, has not been well defined. To probe the mechanisms underlying increased consumption, we identified behavioral changes in rats' licking patterns following NAcc MOR stimulation. Because the temporal structure of licking reflects the physiological substrates modulating consumption, these measures provide a useful tool in dissecting the cause of increased consumption following NAcc MOR stimulation. Next, we used a combination of pharmacological inactivation and lesions to define the role of the VP in hyperphagia following infusion of the MOR-specific agonist [D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) into the NAcc. In agreement with previous studies, results from lick microstructure analysis suggest that NAcc MOR stimulation augments intake through a palatability-driven mechanism. Our results also demonstrate an important role for the VP in normal feeding behavior: pharmacological inactivation of the VP suppresses baseline and NAcc DAMGO-induced consumption. However, this interaction does not occur through a serial circuit requiring direct projections from the NAcc to the VP. Rather, our results indicate that NAcc and VP circuits converge on a common downstream target that regulates food intake.
Authors:
S A Taha; Y Katsuura; D Noorvash; A Seroussi; H L Fields
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2009-03-29
Journal Detail:
Title:  Neuroscience     Volume:  161     ISSN:  1873-7544     ISO Abbreviation:  Neuroscience     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-01     Completed Date:  2009-08-24     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  718-33     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Utah School of Medicine, Salt Lake City, UT 84108, USA. s.taha@utah.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Catheterization
Eating / drug effects,  physiology*
Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / administration & dosage
Feeding Behavior / drug effects,  physiology
GABA Agonists / administration & dosage
Globus Pallidus / drug effects,  physiology*
Hyperphagia / chemically induced,  physiopathology
Male
Motor Activity / drug effects,  physiology
Muscimol / administration & dosage
Neural Pathways / drug effects,  physiology
Neurotoxins / toxicity
Neurotransmitter Agents / administration & dosage
Nucleus Accumbens / drug effects,  physiology*
Quinolinic Acid / toxicity
Random Allocation
Rats
Rats, Long-Evans
Receptors, Opioid, mu / agonists,  metabolism*
Time Factors
Grant Support
ID/Acronym/Agency:
R21 MH082325/MH/NIMH NIH HHS; R21 MH082325-02/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/GABA Agonists; 0/Neurotoxins; 0/Neurotransmitter Agents; 0/Receptors, Opioid, mu; 100929-53-1/Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; 2763-96-4/Muscimol; 89-00-9/Quinolinic Acid
Comments/Corrections

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