Cited by 115Smoking Behavior and CessationNicotinic Acetylcholine Receptors StudySubstance Abuse Treatment and Outcomes

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How does bupropion work as a smoking cessation aid?

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Warner, Charlotte, Shoaib, Mohammed·2005·Addiction Biology

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Abstract

Bupropion exhibits reasonable efficacy as a smoking cessation aid, yet its precise mechanisms of action remain unclear. This review evaluates the mechanism of action of bupropion by considering the clinical evidence in combination with results from pre-clinical experiments in vivo and in vitro. Bupropion is a weak inhibitor of dopamine and noradrenaline reuptake, and has also been shown to antagonise nicotinic acetylcholine receptor function. It is extensively metabolized in humans, its major metabolites reaching levels higher than those of bupropion itself. These metabolites share many of the pharmacological properties of bupropion, so they may play an important role in its clinical activity, yet they have been neglected in investigations into bupropion action. This review led to several conclusions: (1) the principal mode of bupropion action is upon the withdrawal symptoms following smoking cessation; (2) during withdrawal, bupropion may attenuate symptoms by mimicking nicotinic effects on dopamine and noradrenaline; (3) its ability to antagonize nicotinic receptors may prevent relapse by attenuating the reinforcing properties of nicotine, but probably cannot acutely reduce smoking; and (4) further exploration of bupropion metabolites and its role in withdrawal and relapse, within more appropriate animal models, could be crucial in the determination of the precise mechanisms by which bupropion exerts its activity in smoking cessation. Greater elucidation of the exact mechanisms of action of bupropion could lead to the development of new drugs even more beneficial in promoting smoking abstinence.

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Authors: Warner, C., & Shoaib, M.
Affiliations: Newcastle University (GB)
Corresponding author: Shoaib, Mohammed
ORCID: Warner, Charlotte
Shoaib, Mohammed
Venue: Addiction Biology
Publisher: Wiley
Published: 2005-09
Volume: 10
Issue: 3
Pages: 219-231
ISSN: 1355-6215 (ISSN-L)
1369-1600
DOI: 10.1080/13556210500222670
OpenAlex: W2042273131
Cited by: 115
References: 54
Citations by year: 2026: 2 · 2025: 5 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 2 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 7 · 2016: 7 · 2015: 12 · 2014: 3 · 2013: 3 · 2012: 2
FWCI: 1.38
Type: journal article
Language: en
Open access: green
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 281 d)
Locations: Addiction Biology (publishedVersion)
PubMed (publishedVersion)
Newcastle University ePrints (Newcastle Univesity)
Topics: Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
Keywords: bupropion, smoking cessation, mechanism of action, nicotine withdrawal symptoms, nicotinic acetylcholine receptor antagonism, dopamine uptake inhibition, norepinephrine reuptake inhibition, nicotine reinforcement, smoking abstinence
MeSH terms: Smoking Prevention, Administration, Cutaneous, Dopamine, Double-Blind Method, Humans, Nicotine, Norepinephrine, Receptors, Nicotinic, Substance Withdrawal Syndrome, Smoking Cessation, Bupropion, Dopamine Uptake Inhibitors

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