Document Detail


Recent advances in understanding nicotinic receptor signaling mechanisms that regulate drug self-administration behavior.
MedLine Citation:
PMID:  21740894     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tobacco smoking is one of the leading causes of disease and premature death in the United States. Nicotine is considered the major reinforcing component in tobacco smoke responsible for tobacco addiction. Nicotine acts in the brain through the neuronal nicotinic acetylcholine receptors (nAChRs). The predominant nAChR subtypes in mammalian brain are those containing α4 and β2 subunits. The α4β2 nAChRs, particularly those located in the mesoaccumbens dopamine pathway, play a key role in regulating the reinforcing properties of nicotine. Considering that twelve mammalian nAChR subunits have been cloned, it is likely that nAChRs containing subunits in addition to, or other than, α4 and β2 also play a role in the tobacco smoking habit. Consistent with this possibility, human genome-wide association studies have shown that genetic variation in the CHRNA5-CHRNA3-CHRNB4 gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to tobacco addiction and smoking-related diseases. Most recently, α5-containing nAChRs located in the habenulo-interpeduncular tract were shown to limit intravenous nicotine self-administration behavior in rats and mice, suggesting that deficits in α5-containing nAChR signaling in the habenulo-interpeduncular tract increases vulnerability to the motivational properties of nicotine. Finally, evidence suggests that nAChRs may also play a prominent role in controlling consumption of addictive drugs other than nicotine, including cocaine, alcohol, opiates and cannabinoids. The aim of the present review is to discuss recent preclinical findings concerning the identity of the nAChR subtypes that regulate self-administration of nicotine and other drugs of abuse.
Authors:
Luis M Tuesta; Christie D Fowler; Paul J Kenny
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-06-29
Journal Detail:
Title:  Biochemical pharmacology     Volume:  82     ISSN:  1873-2968     ISO Abbreviation:  Biochem. Pharmacol.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-08-25     Completed Date:  2011-10-21     Revised Date:  2014-02-03    
Medline Journal Info:
Nlm Unique ID:  0101032     Medline TA:  Biochem Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  984-95     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Behavior, Animal / drug effects
Brain / drug effects,  metabolism
Ethanol / administration & dosage,  pharmacology*
Humans
Nicotine / administration & dosage,  pharmacology*
Protein Subunits
Receptors, Nicotinic / genetics,  metabolism*
Reinforcement (Psychology)
Self Administration
Signal Transduction / drug effects*
Street Drugs / pharmacology*
Grant Support
ID/Acronym/Agency:
DA020686/DA/NIDA NIH HHS; DA026693/DA/NIDA NIH HHS; DA032225/DA/NIDA NIH HHS; F31 DA032225-01/DA/NIDA NIH HHS; F32 DA026693/DA/NIDA NIH HHS; R01 DA020686-05/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/Protein Subunits; 0/Receptors, Nicotinic; 0/Street Drugs; 3K9958V90M/Ethanol; 54-11-5/Nicotine
Comments/Corrections

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


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