Involvement of neuronal β2 subunit‐containing nicotinic acetylcholine receptors in nicotine reward and withdrawal: Implications for pharmacotherapies. (14th May 2014)

• Record Type: Journal Article
• Authors: Simmons, Steven J.; Gould, Thomas J.
• Is Part Of: Journal of clinical pharmacy and therapeutics. Volume 39:Number 5(2014:Oct.)
• Page Start: 457
• Page End: 467
• Publication Date: 2014-05-14
• Subjects: Clinical pharmacology -- Periodicals; Chemotherapy -- Periodicals; 615
• DOI: 10.1111/jcpt.12171
• Languages: English
• ISSNs: 0269-4727

Abstract

<abstract abstract-type="main" id="jcpt12171-abs-0001"> <title>Summary</title> <sec id="jcpt12171-sec-0001" sec-type="section"> <title>What is known and objective</title> <p>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.</p> </sec> <sec id="jcpt12171-sec-0002" sec-type="section"> <title>Comment</title> <p>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.</p> </sec> <sec id="jcpt12171-sec-0003" sec-type="section"> <title>What is new and conclusion</title> <p>Smoking cessation pharmacotherapies act on β₂ subunit‐containing nAChRs to reduce nicotine reward and withdrawal symptom severity.</p> </sec> </abstract>