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Link to original content: https://pubmed.ncbi.nlm.nih.gov/23545467/
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Review
. 2013 Aug;23(4):493-9.
doi: 10.1016/j.conb.2013.02.013. Epub 2013 Mar 29.

Unraveling the neurobiology of nicotine dependence using genetically engineered mice

Astrid K Stoker  1 , Athina Markou
Affiliations
Review

Unraveling the neurobiology of nicotine dependence using genetically engineered mice

Astrid K Stoker et al. Curr Opin Neurobiol. 2013 Aug.

Abstract

This review article provides an overview of recent studies of nicotine dependence and withdrawal that used genetically engineered mice. Major progress has been made in recent years with mutant mice that have knockout and gain-of-function of specific neuronal nicotinic acetylcholine receptor (nAChR) subunit genes. Nicotine exerts its actions by binding to neuronal nAChRs that consist of five subunits. The different nAChR subunits that combine to compose a receptor determine the distinct pharmacological and kinetic properties of the specific nAChR. Recent findings in genetically engineered mice have indicated that while α4-containing and β2-containing nAChRs are involved in the acquisition of nicotine self-administration and initial stages of nicotine dependence, α7 homomeric nAChRs appear to be involved in the later stages of nicotine dependence. In the medial habenula, α5-containing, α3-containing, and β4-containing nAChRs were shown to be crucially important in the regulation of the aversive aspects of nicotine. Studies of the involvement of α6 nAChR subunits in nicotine dependence have only recently emerged. The use of genetically engineered mice continues to vastly improve our understanding of the neurobiology of nicotine dependence and withdrawal.

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Conflict of interest statement

Conflict of Interest

AM has received contract research support from Bristol-Myers Squibb Co. and honoraria/consulting fees from Abbott GmbH and Company, AstraZeneca, and Pfizer during the past 2 years. AM has a patent on the use of metabotropic glutamate compounds for the treatment of nicotine dependence.

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