Bupropion (English Wikipedia)

Analysis of information sources in references of the Wikipedia article "Bupropion" in English language version.

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  • Hailwood JM (27 September 2018). Novel approaches towards pharmacological enhancement of motivation (Thesis). University of Cambridge. pp. 13–14. doi:10.17863/CAM.40216. 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.

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  • "Bupropion". PubChem. United States National Library of Medicine – National Center for Biotechnology Information. 28 July 2018. Archived from the original on 29 July 2018. Retrieved 29 July 2018.
  • "Bupropion – Biological Test Results". PubChem. U.S. National Library of Medicine. Retrieved 19 August 2024.
  • "Bupropion". PubChem. Retrieved 4 August 2024.

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  • Roth BL, Driscol J. "Bupropion – PDSP Ki Database". Psychoactive Drug Screening Program (PDSP). University of North Carolina at Chapel Hill and the United States National Institute of Mental Health. Retrieved 19 August 2024.

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  • Hamati R (10 January 2020). Investigating the Potential Role of Serotonin-2B Receptor Antagonism in the Neuronal Actions of Adjunctive Aripiprazole (M.Sc. thesis). doi:10.20381/RUOR-24287. 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).

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