How does bupropion work as a smoking cessation aid?
Open accessAbstract
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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The anti-smoking properties of bupropion may depend on its ability to substitute some psychomotor and/or reinforcement-related effects of nicotine.
“Therefore, the anti-smoking properties of bupropion may depend on its ability to substitute some of the psychomotor and/or reinforcement-related effects of nicotine [232].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [232]
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- Authors
- Warner, C., & Shoaib, M.
- Affiliations
- Newcastle University (GB)
- Corresponding author
- Shoaib, Mohammed
- Venue
- Addiction Biology
- Publisher
- Wiley
- Published
- 2005-09
- Volume
- 10
- Issue
- 3
- Pages
- 219-231
- ISSN
- 1355-6215 (ISSN-L)
- 1369-1600
- 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
- Locations
- Addiction Biology (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Topics
- Health Sciences › Medicine › Physiology › 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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