Literature DB >> 24828779

Involvement of neuronal β2 subunit-containing nicotinic acetylcholine receptors in nicotine reward and withdrawal: implications for pharmacotherapies.

Steven J Simmons1, Thomas J Gould.   

Abstract

WHAT IS KNOWN AND
OBJECTIVE: Tobacco smoking remains a major health problem. Nicotine binds to nicotinic acetylcholine receptors (nAChRs), which can cause addiction and withdrawal symptoms upon cessation of nicotine administration. Pharmacotherapies for nicotine addiction target brain alterations that underlie withdrawal symptoms. This review will delineate the involvement of the β2 subunit of neuronal nAChRs in nicotine reward and in generating withdrawal symptoms to better understand the efficacy of smoking cessation pharmacotherapies. COMMENT: Chronic nicotine desensitizes and upregulates β2 subunit-containing nAChRs, and the prolonged upregulation of receptors may underlie symptoms of withdrawal. Experimental research has demonstrated that the β2 subunit of neuronal nAChRs is necessary for generating nicotine reward and withdrawal symptoms. WHAT IS NEW AND
CONCLUSION: Smoking cessation pharmacotherapies act on β2 subunit-containing nAChRs to reduce nicotine reward and withdrawal symptom severity.
© 2014 John Wiley & Sons Ltd.

Entities:  

Keywords:  nicotine reward; nicotine withdrawal; nicotinic acetylcholine receptor; smoking cessation; β2 subunit

Mesh:

Substances:

Year:  2014        PMID: 24828779      PMCID: PMC4459499          DOI: 10.1111/jcpt.12171

Source DB:  PubMed          Journal:  J Clin Pharm Ther        ISSN: 0269-4727            Impact factor:   2.512


  182 in total

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6.  Reappraising Choice in Addiction: Novel Conceptualizations and Treatments for Tobacco Use Disorder.

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