J Clin Psychopharmacol. 2004 Jun;24(3):339-342.
Bupropion Sustained Release for the Treatment of Hypoactive Sexual Desire Disorder in Premenopausal Women.

Segraves RT, Clayton A, Croft H, Wolf A, Warnock J.

*Department of Psychiatry, Case Western Reserve University and Metro-Health Medical System, Cleveland, OH; daggerDepartment of Psychiatry, University of Virginia, Charlottesville, VA; double daggerSan Antonio, TX; section signDepartment of Psychiatry, University of Oklahoma, Oklahoma City, OK.

: Premenopausal women meeting operational criteria for idiopathic, acquired, global hypoactive sexual desire disorder were studied in a randomized, double-blind, placebo-controlled, multiple-site escalating dose 112-day trial of bupropion sustained release. Outcome was measured by investigator-rating and self-administered questionnaires. All measures indicated greater sexual responsiveness in women receiving bupropion. The Changes in Sexual Functioning Questionnaire indicated that bupropion had significant effects on increasing measures of sexual arousal, orgasm completion, and sexual satisfaction.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15118489&dopt=Abstract Bupropion Wellbutrin




Int J Neuropsychopharmacol. 2004 Apr 26;:1-7. [Epub ahead of print]
Effect of treatment with bupropion on EEG sleep: relationship to antidepressant response.

Ott GE, Rao U, Lin KM, Gertsik L, Poland RE.

Interdepartmental Training Program for Neuroscience, UCLA, CA, USA.

The objective of this study was to assess whether treatment with sustained-release bupropion (Wellbutrin-SR) produces alterations in electroencephalographic (EEG) sleep that are associated with clinical response to the drug. EEG sleep was measured in 20 patients with unipolar major depressive disorder before and after treatment with sustained-release bupropion. Each EEG sleep session consisted of two consecutive nights. Treatment with bupropion lasted for 8 wk. Compared to EEG sleep measures at baseline, treatment with bupropion significantly lengthened REM latency, increased REM activity and density during the first REM period, and increased total REM density. Differential response to treatment was associated with changes in REM activity and density, but not with REM latency. However, in contrast to many other antidepressants, REM sleep was not suppressed.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15122973&dopt=Abstract Bupropion Wellbutrin




Neuropharmacology. 2002 Feb;42(2):181-90.
Influence of fluoxetine on the ability of bupropion to modulate extracellular dopamine and norepinephrine concentrations in three mesocorticolimbic areas of rats.

Li SX, Perry KW, Wong DT.

Neuroscience Research, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285, USA.

The finding that serotonin (5-HT) can modulate dopamine (DA) and norepinephrine (NE) release in the brain has led us to hypothesize that fluoxetine, a selective 5-HT reuptake inhibitor, may influence the ability of bupropion, a preferential DA and NE dual reuptake inhibitor, to modulate extracellular DA and NE concentrations in some brain areas. The present study was designed to evaluate this hypothesis by assessing the effects of fluoxetine on bupropion-induced changes in extracellular monoamine concentrations by means of in vivo microdialysis. Three mesocorticolimbic areas including hypothalamus (Ht), prefrontal cortex (Pfc) and nucleus accumbens (Acb) were selected based on their relevance to depression and antidepressant actions. In the Ht of untreated rats, bupropion dose-dependently (s.c.) increased extracellular DA and NE concentrations either in single injection study or in sequential injection study. Thus, 10 mg/kg of bupropion had no effect on the DA and NE concentrations, while 30 mg/kg of bupropion induced transient but significant increases (about 240% of the baselines), and 100 mg/kg of bupropion induced marked and persistent increases (over 600% of the baselines) in the DA and NE concentrations. In the rats pre-treated with fluoxetine (10 mg/kg, s.c., 90 min interval), the threshold dose of bupropion (10 mg/kg) significantly increased the DA and NE concentrations to more than 350% of the baselines, and 30 mg/kg of bupropion markedly increased the DA and NE concentrations to more than 570% of the baselines in the Ht. The fluoxetine pre-treatment also potentiated the DA increases induced by 10 mg/kg of bupropion in the Pfc (260% for bupropion alone vs

utsouthwestern.edu

OBJECTIVE: To examine the effects of bupropion sustained release (SR) and sertraline on anxiety in outpatients with recurrent DSM-IV-defined major depressive disorder. METHOD: This retrospective analysis was conducted using pooled data from 2 identical, 8-week, acute-phase, double-blind, placebo-controlled, parallel-group studies of bupropion SR (N = 234), sertraline (N = 225), and placebo (N = 233). Symptoms of anxiety and depression were measured using the 14-item Hamilton Rating Scale for Anxiety (HAM-A) and the 21-item Hamilton Rating Scale for Depression (HAM-D-21), respectively. Percentage reduction in baseline HAM-A total score for each treatment week was calculated to determine whether the time to onset of anxiolytic activity differed among antidepressant responders to each agent. Central nervous system (CNS) adverse events were tabulated. RESULTS: Bupropion SR and sertraline were comparably effective, both were superior to placebo in reducing depressive symptoms. and they did not differ in their effect on anxiety symptoms. Antidepressant responders (> 50% reduction in baseline HAM-D-21 score) in both groups showed marked and comparable reductions in HAM-A scores (baseline to exit). There were no differences between bupropion SR and sertraline in the median time (4 weeks) to reach a clinically significant anxiolytic effect (> or = 50% reduction in baseline HAM-A score). CNS adverse events were comparable for bupropion SR and sertraline, except for somnolence, which was more common in sertraline-treated patients. CONCLUSION: Bupropion SR and sertraline had comparable antidepressant and anxiolytic effects and an equally rapid onset of clinically

partners.org

OBJECTIVE: To examine treatment practices in cases where selective serotonin reuptake inhibitors (SSRIs) are ineffective. METHODS: We surveyed 801 clinicians (including 630 psychiatrists) attending the Massachusetts General Hospital's annual psychopharmacology review course. Clinicians were presented with a vignette about a patient with depression who had responded partially to an SSRI and were asked to choose among various strategies available to manage this patient. RESULTS: Of those surveyed, 466 clinicians had been in practice a mean of 16.6 years (SD 10.7). Not all clinicians chose to answer every question. Among 455 respondents, 84% (n = 382) chose to increase the dose of the SSRI, 10% (n = 47) chose augmentation or combination, and 7% (n = 31) opted for switching agents. When asked to switch to another agent, 448 responded, of whom 52% (n = 235) chose a newer antidepressant, 34% (n = 152) chose another SSRI, 10% (n = 44) chose a tricyclic antidepressant (TCA), 2% (n = 8) chose a serotonin norepinephrine reuptake inhibitor (SNRI), 1% (n = 5) chose a monoamine oxidase inhibitor (MAOI), and 1% (n = 4) chose an undefined "other" agent. Among 445 respondents, bupropion was the most widely chosen augmenting agent (30%, n = 134), followed by lithium (22%, n = 98). West coast and Canadian clinicians preferred to switch to another SSRI rather than to a newer antidepressant. Canadian clinicians preferred lithium to bupropion as their first-choice augmenting agent, as did clinicians from academic settings. Clinicians from community, individual practice, or group settings favoured bupropion. More experienced clinicians preferred bupropion as a fir