| Recent advances in understanding nicotinic receptor signaling mechanisms that regulate drug self-administration behavior. | |
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MedLine Citation:
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PMID: 21740894 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Luis M Tuesta; Christie D Fowler; Paul J Kenny |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2011-06-29 |
Journal Detail:
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Title: Biochemical pharmacology Volume: 82 ISSN: 1873-2968 ISO Abbreviation: Biochem. Pharmacol. Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-08-25 Completed Date: 2011-10-21 Revised Date: 2013-05-24 |
Medline Journal Info:
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Nlm Unique ID: 0101032 Medline TA: Biochem Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 984-95 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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Laboratory of Behavioral and Molecular Neuroscience, Department of Molecular Therapeutics, The Scripps Research Institute - Scripps Florida, Jupiter, FL 33458, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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DA020686/DA/NIDA NIH HHS; DA026693/DA/NIDA NIH HHS; DA032225/DA/NIDA NIH HHS; F31 DA032225-01/DA/NIDA NIH HHS; R01 DA020686-05/DA/NIDA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Protein Subunits; 0/Receptors, Nicotinic; 0/Street Drugs; 54-11-5/Nicotine; 64-17-5/Ethanol |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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