Analysis of information sources in references of the Wikipedia article "Bupropion" in English language version.
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Bupropion also acts as a dopamine reuptake inhibitor (Dwoskin et al. 2006), and has been used as a treatment for depression as well as a smoking cessation aid (Stahl et al. 2004). Bupropion has been shown to produce a dose-dependent increase in PR breakpoints (Bruijnzeel & Markou 2003). Furthermore, systemic administration of bupropion increases the selection of the high-effort, high-reward option in a PR-choice task in rats (Randall, Lee, Podurgiel, et al. 2014). Bupropion is also effective at rescuing motivational impairments in rodents. Administration of bupropion can rescue deficits in effort-related decision-making induced by pre-treatment with tetrabenazine (Randall, Lee, Nunes, et al. 2014; Nunes, Randall, Hart, et al. 2013) and the pro-inflammatory cytokine interleukin-6 (Yohn, Arif, et al. 2016). Bupropion has been reported to improve symptoms of apathy in cases of acquired brain injury, major depression (Corcoran et al. 2004), and frontotemporal dementia (Lin et al. 2016). | However, several larger placebo-controlled studies suggest only limited effects of bupropion. In a study of 40 patients with schizophrenia, bupropion was found to have no significant effect on apathy or negative symptoms as a whole (Yassini et al. 2014). Furthermore, in a recent RCT of bupropion in HD, apathy was not significantly affected by the drug (Gelderblom et al. 2017). | It is not clear whether bupropion lacks clinical efficacy, whether bupropion as a whole is not effective at treating motivational impairments, or is not effective in the clinical populations tested.
{{cite journal}}: CS1 maint: DOI inactive as of March 2026 (link)Bupropion also acts as a dopamine reuptake inhibitor (Dwoskin et al. 2006), and has been used as a treatment for depression as well as a smoking cessation aid (Stahl et al. 2004). Bupropion has been shown to produce a dose-dependent increase in PR breakpoints (Bruijnzeel & Markou 2003). Furthermore, systemic administration of bupropion increases the selection of the high-effort, high-reward option in a PR-choice task in rats (Randall, Lee, Podurgiel, et al. 2014). Bupropion is also effective at rescuing motivational impairments in rodents. Administration of bupropion can rescue deficits in effort-related decision-making induced by pre-treatment with tetrabenazine (Randall, Lee, Nunes, et al. 2014; Nunes, Randall, Hart, et al. 2013) and the pro-inflammatory cytokine interleukin-6 (Yohn, Arif, et al. 2016). Bupropion has been reported to improve symptoms of apathy in cases of acquired brain injury, major depression (Corcoran et al. 2004), and frontotemporal dementia (Lin et al. 2016). | However, several larger placebo-controlled studies suggest only limited effects of bupropion. In a study of 40 patients with schizophrenia, bupropion was found to have no significant effect on apathy or negative symptoms as a whole (Yassini et al. 2014). Furthermore, in a recent RCT of bupropion in HD, apathy was not significantly affected by the drug (Gelderblom et al. 2017). | It is not clear whether bupropion lacks clinical efficacy, whether bupropion as a whole is not effective at treating motivational impairments, or is not effective in the clinical populations tested.
Case reports in youths have noted exacerbation or new onset of tics and repetitive compulsive behaviors [41,42].
Although the mechanism of action of bupropion is not fully understood, DAT inhibition is unlikely because four positron emission tomography (PET) scan studies have reported that clinically effective doses of bupropion produce very low occupancy of dopamine reuptake sites [113, 114, 115, 116]. It is unlikely that such low DAT occupancy has an effect on DA transmission since the value obtained is hardly different from baseline [113]. Moreover, a lack of NE reuptake inhibition is indicated by its lack of inhibitory effect on the tyramine pressor response, contrarily to NRIs [117].
There is controversy regarding the property of bupropion to inhibit reuptake of NET and DAT at clinically relevant doses. The 80% rule-of-thumb states that neurological and mental illness arises with loss of approximately 80% of neurotransmitter nuclei (i.e. substantia nigra, nucleus basalis). In parallel, SSRIs exert therapeutic their effect by occupying 80% of 5-HTT (Meyer et al., 2007) and provides the rational that the monoamine systems are resilient and require significant alterations in their function to produce clinically relevant effects (Blier, 2008). In contrast, therapeutically relevant doses of bupropion occupy 15-25% of DAT and do not alter responses on the tyramine pressor test (a proxy of NET inhibition; Gobbi et al., 2003; Stahl et al., 2004). Thus, bupropion might not be exerting its effects through DAT or NET inhibition but rather acts as a DA and NE releaser (Gobbi et al., 2003; Blier, 2008).
Either a decrease in the pressor response to the same doses of tyramine, or an increase in the dose of tyramine necessary to cause a given increase in systolic BP, is considered to be a reliable index of NE reuptake blockade. [...] The robust inhibitory action of desipramine on the tyramine pressor response was expected based on prior reports from ours, and several other laboratories. Indeed, amitriptyline and imipramine (which are metabolized to nortriptyline and desipramine respectively) potently inhibit this response, as does nortriptyline itself, maproptiline, clomipramine (which is metabolized to the potent NE reuptake inhibitor desmethyl-clomipramine), and the nontricyclic NE reuptake inhibitors tomoxetine (now denoted atomoxetine) and reboxetine (Gobbi et al., 2003; Harvey et al., 2000; Hassan et al., 1985, 1989; Seppala et al., 1981; Slater et al., 2000; Turcotte et al., 2001; Zerbe et al., 1985).
AXS-05 is a combination of dextromethorphan and bupropion and has been shown to have a rapid (within one week) positive effect in patients with depression. Dextromethorphan, as described above as part of Nuedexta, is a σ-1R agonist, an NMDA antagonist, and has an affinity for the serotonin reuptake transporter. Whereas, bupropion is a moderately effective antidepressant when taken alone, thought to act by preventing dopamine and noradrenaline reuptake [230]. Studies in mice have shown that the antidepressant-like effects of bupropion are potentiated by σ-1R agonists, and inhibited by σ-1R antagonists [231]. These findings suggest that the combination of a σ-1R agonist and the dopamine/ noradrenaline reuptake inhibitor will be more effective than either treatment alone.
Many stimulants have potency at the rat TAAR1 in the micromolar range but tend to be about 5 to 10 times less potent at the human TAAR1, but bupropion was found to be inactive.87,88
In vitro functional studies showed agonist activity of solriamfetol at human, mouse, and rat TAAR1 receptors. hTAAR1 EC50 values (10–16 μM) were within the clinically observed therapeutic solriamfetol plasma concentration range and overlapped with the observed DAT/NET inhibitory potencies of solriamfetol in vitro. TAAR1 agonist activity was unique to solriamfetol; neither the WPA modafinil nor the DAT/NET inhibitor bupropion had TAAR1 agonist activity.
Bupropion, the N-tert-butyl analog of 3-chlorocathinone, is a clinically employed antidepressant.
Эфедрон (меткатинон) и его производные, за исключением производных, включенных в качестве самостоятельных позиций в перечень Ephedrone (methcathinone) and its derivatives, with the exception of derivatives included as independent items in the list.
{{cite journal}}: CS1 maint: DOI inactive as of March 2026 (link)Case reports in youths have noted exacerbation or new onset of tics and repetitive compulsive behaviors [41,42].
Finally, case reports12,14 suggest some possible adverse effects of bupropion use. These include possible exacerbation or new manifestation of tics that resolve after bupropion is withdrawn, the development of repetitive and compulsive behaviors in patients who may be vulnerable to the development of obsessive-compulsive disorder (OCD) and/or tics, and, in one case, hypomanic symptoms.
Although the mechanism of action of bupropion is not fully understood, DAT inhibition is unlikely because four positron emission tomography (PET) scan studies have reported that clinically effective doses of bupropion produce very low occupancy of dopamine reuptake sites [113, 114, 115, 116]. It is unlikely that such low DAT occupancy has an effect on DA transmission since the value obtained is hardly different from baseline [113]. Moreover, a lack of NE reuptake inhibition is indicated by its lack of inhibitory effect on the tyramine pressor response, contrarily to NRIs [117].
Either a decrease in the pressor response to the same doses of tyramine, or an increase in the dose of tyramine necessary to cause a given increase in systolic BP, is considered to be a reliable index of NE reuptake blockade. [...] The robust inhibitory action of desipramine on the tyramine pressor response was expected based on prior reports from ours, and several other laboratories. Indeed, amitriptyline and imipramine (which are metabolized to nortriptyline and desipramine respectively) potently inhibit this response, as does nortriptyline itself, maproptiline, clomipramine (which is metabolized to the potent NE reuptake inhibitor desmethyl-clomipramine), and the nontricyclic NE reuptake inhibitors tomoxetine (now denoted atomoxetine) and reboxetine (Gobbi et al., 2003; Harvey et al., 2000; Hassan et al., 1985, 1989; Seppala et al., 1981; Slater et al., 2000; Turcotte et al., 2001; Zerbe et al., 1985).
AXS-05 is a combination of dextromethorphan and bupropion and has been shown to have a rapid (within one week) positive effect in patients with depression. Dextromethorphan, as described above as part of Nuedexta, is a σ-1R agonist, an NMDA antagonist, and has an affinity for the serotonin reuptake transporter. Whereas, bupropion is a moderately effective antidepressant when taken alone, thought to act by preventing dopamine and noradrenaline reuptake [230]. Studies in mice have shown that the antidepressant-like effects of bupropion are potentiated by σ-1R agonists, and inhibited by σ-1R antagonists [231]. These findings suggest that the combination of a σ-1R agonist and the dopamine/ noradrenaline reuptake inhibitor will be more effective than either treatment alone.
Many stimulants have potency at the rat TAAR1 in the micromolar range but tend to be about 5 to 10 times less potent at the human TAAR1, but bupropion was found to be inactive.87,88
Drugs that are found to mimic the stimulus, but not reinforcing effects of cocaine in monkeys might have a role as pharmacological adjuncts for the treatment of cocaine withdrawal in people. By partially substituting for cocaine, such drugs could help alleviate the subjective symptoms of cocaine abstinence (e.g., craving) without themselves promoting abuse. [...] Other candidates include bupropion and the experimental compounds SKF 81297, Lu 19005, and quinelorane (Table 1), all of which substitute at least partially for cocaine in drug-discrimination experiments with monkeys (Melia et al., 1989; Spealman et al., 1991b, unpublished observations). Bupropion has been found to maintain i.v. self-administration in monkeys (Bergman et al., 1989) and thus may have reinforcing effects by this route in people. Orally, however, bupropion is thought to have minimal abuse liability at recommended therapeutic doses.
Bupropion, the N-tert-butyl analog of 3-chlorocathinone, is a clinically employed antidepressant.
{{cite journal}}: CS1 maint: DOI inactive as of March 2026 (link)Although the mechanism of action of bupropion is not fully understood, DAT inhibition is unlikely because four positron emission tomography (PET) scan studies have reported that clinically effective doses of bupropion produce very low occupancy of dopamine reuptake sites [113, 114, 115, 116]. It is unlikely that such low DAT occupancy has an effect on DA transmission since the value obtained is hardly different from baseline [113]. Moreover, a lack of NE reuptake inhibition is indicated by its lack of inhibitory effect on the tyramine pressor response, contrarily to NRIs [117].
Bupropion, the N-tert-butyl analog of 3-chlorocathinone, is a clinically employed antidepressant.
There is controversy regarding the property of bupropion to inhibit reuptake of NET and DAT at clinically relevant doses. The 80% rule-of-thumb states that neurological and mental illness arises with loss of approximately 80% of neurotransmitter nuclei (i.e. substantia nigra, nucleus basalis). In parallel, SSRIs exert therapeutic their effect by occupying 80% of 5-HTT (Meyer et al., 2007) and provides the rational that the monoamine systems are resilient and require significant alterations in their function to produce clinically relevant effects (Blier, 2008). In contrast, therapeutically relevant doses of bupropion occupy 15-25% of DAT and do not alter responses on the tyramine pressor test (a proxy of NET inhibition; Gobbi et al., 2003; Stahl et al., 2004). Thus, bupropion might not be exerting its effects through DAT or NET inhibition but rather acts as a DA and NE releaser (Gobbi et al., 2003; Blier, 2008).
Эфедрон (меткатинон) и его производные, за исключением производных, включенных в качестве самостоятельных позиций в перечень Ephedrone (methcathinone) and its derivatives, with the exception of derivatives included as independent items in the list.
In vitro functional studies showed agonist activity of solriamfetol at human, mouse, and rat TAAR1 receptors. hTAAR1 EC50 values (10–16 μM) were within the clinically observed therapeutic solriamfetol plasma concentration range and overlapped with the observed DAT/NET inhibitory potencies of solriamfetol in vitro. TAAR1 agonist activity was unique to solriamfetol; neither the WPA modafinil nor the DAT/NET inhibitor bupropion had TAAR1 agonist activity.