Sustained administration of bupropion alters the neuronal activity of serotonin, norepinephrine but not dopamine neurons in the rat brain
Abstract
Bupropion is widely used in the treatment of depression. There are, however, limited data on its long-term effects on monoaminergic neurons and therefore the mechanism of its delayed onset of action is at present not well understood. The present study was conducted to examine the effects of prolonged bupropion administration on the firing activity of dorsal raphe nucleus (DRN), locus coeruleus (LC), and ventral tegmental area (VTA) neurons. Spontaneously firing neurons were recorded extracellularly in rats anesthetized with chloral hydrate. Bupropion (30 mg/kg/day) was administered using subcutaneously implanted minipumps. In the DRN, the firing rate of serotonin (5-HT) neurons was significantly increased after 2, 7 and 14 days of administration. The suppressant effect of LSD was significantly diminished after the two-day regimen, indicating a desensitization of 5-HT1A autoreceptors. In the LC, the firing rate of norepinephrine (NE) neurons was significantly attenuated after a 2-day regimen, but recovered progressively over 14 days of administration. The suppressant effect of clonidine on NE neuronal firing was significantly attenuated in rats treated with bupropion for 14 days, indicating a desensitization of alpha2-adrenoceptors. In the VTA, neither 2 nor 14 days of bupropion administration altered the firing and burst activity of dopamine neurons. These results indicate that bupropion, unlike 5-HT reuptake inhibitors, promptly increased 5-HT neuronal activity, due to early desensitization of the 5-HT1A autoreceptor. The gradual recovery of neuronal firing of NE neurons, due to the desensitization of alpha2-adrenoceptors, in the presence of the sustained increase in 5-HT neuronal firing, may explain in part the delayed onset of action of bupropion in major depression.
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Bupropion may increase NE levels in the dorsal raphe nucleus, leading to increased 5-HT levels.
“The drug may also function by increasing NE levels in the dorsal raphe nucleus, thus leading to increased serotonin (5-HT) levels [217].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [217]
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Sinton, C. M., & McCarley, R. W. (2011) · Cambridge University Press eBooks · doi:10.1017/cbo9781139042734.006
Heysieattalab, S., Zare, S., Pakdel, F. G., & Hashtjini, M. M. (2010) · Iranian journal of basic medical sciences. · doi:10.22038/ijbms.2010.5114
“Bupropion can increase extracellular dopamine and norepinephrine concentrations in mesocorticolimbic areas without influencing serotonin concentration (6-8).”
BackgroundEfectos del bupropión sobre depresión, ansiedad y abstinencia a nicotina
Hernández-Lozano, M., Gutiérrez‐García, A. G., Contreras, C. M., & López, G. A. (2010) · Archivos de Neurociencias
Iskandarani, E., & Kareem, S. (2014) · uO Research (University of Ottawa) · doi:10.20381/ruor-3466
Impact of Medications Used in the Treatment of Mood Disorders on Monoaminergic Systems
Ghanbari, R. (2011) · Library and Archives Canada (Government of Canada) · doi:10.20381/ruor-4467
“…hatched arrows on the 5-HT and NE cell bodies correspond to the diminished sensitivity of somatodendritic 5-HT1A and α2-adrenergic autoreceptors (El Mansari et al., 2008; Ghanbari et al., 2010), presynaptic α2-adrenergic auto- and heteroreceptors on NE and 5-HT terminals, and the diminished…”
BackgroundHerman, A. (2017) · uO Research (University of Ottawa) · doi:10.20381/ruor-20993
“…receptors, and the inhibitory effect of NE on DA neurons occurs through α2-adrenergic receptors as well, although the evidence is less clear regarding the latter, and there is additional evidence of an enhancing effect through α1 -adrenoceptors (El Mansari et al, 2008; El Mansari et al, 2010).”
BackgroundCamacho, M. B. (2018) · Illinois Digital Environment for Access to Learning and Scholarship (University of Illinois at Urbana-Champaign)
Hamati, R. (2020) · uO Research (University of Ottawa) · doi:10.20381/ruor-24287
“Furthermore, the hypothesis that bupropion is a DA releaser rather than a DAT inhibitor is indicated by a lack of effect on DA firing at any time-point and increases in DA levels in several brain areas, respectively (Li et al., 2002; El Mansari et al., 2008).”
BackgroundIn Response to Borgsteede et al. About Bupropion and Serotonin Toxicity
Murray, B. P., Carpenter, J. E., Moran, T. P., Calello, D. P., & Kazzi, Z. (2020) · Journal of Medical Toxicology · doi:10.1007/s13181-020-00764-w
Otto, S., Horneber, M., & Weis, J. (2023) · Springer eBooks · doi:10.1007/978-3-662-64615-1_4
Acute Colonic Pseudo-obstruction Following Massive Bupropion Overdose
Johnson, M., GALES, J., Gronbeck, K. R., & STEINWEHR, D. (2026) · Journal of Investigative Medicine High Impact Case Reports · doi:10.1177/23247096261479684
Mansari, M. E., Okamoto, N., & Blier, P. (2026) · Journal of Psychopharmacology · doi:10.1177/02698811261478602
- Authors
- El Mansari, M., Ghanbari, R., Janssen, S., & Blier, P.
- Affiliations
- University of Ottawa (CA)
- University of Florida (US)
- ORCID
- Blier, Pierre
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 55
- Issue
- 7
- Pages
- 1191-1198
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2053556318
- Cited by
- 63
- References
- 41
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 2 · 2021: 1 · 2020: 8 · 2019: 3 · 2018: 2 · 2017: 3 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 5
- FWCI
- 3.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Ottawa
- Government of Canada
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- bupropion, serotonergic neurons, noradrenergic neurons, dopaminergic neurons, dorsal raphe nucleus, locus coeruleus, ventral tegmental area, spontaneous neuronal firing, major depressive disorder, monoaminergic neurons
- MeSH terms
- Animals, Dopamine, Electrophysiology, Locus Coeruleus, Male, Neurons, Norepinephrine, Raphe Nuclei, Serotonin, Bupropion, Rats, Sprague-Dawley, Ventral Tegmental Area, Receptors, Adrenergic, alpha-2, Dopamine Uptake Inhibitors, Receptor, Serotonin, 5-HT1A, Rats
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