Drugs online research references
J Clin Psychiatry. 1993 Dec;54(12):459-65.
Improvement in fluoxetine-associated sexual dysfunction in patients switched to bupropion.
Walker PW, Cole JO, Gardner EA, Hughes AR, Johnston JA, Batey SR, Lineberry CG.
Department of Psychiatry, University of Tennessee, Memphis.
BACKGROUND: This study was conducted to determine the effect of bupropion on the sexual functioning of male and female outpatients who developed anorgasmia or delayed orgasm while receiving fluoxetine treatment for depression. METHOD: Thirty-nine patients who satisfied criteria for participation in the study discontinued fluoxetine treatment and entered a 2-week washout phase followed by an open 8-week bupropion treatment phase. Three parameters of sexual functioning were followed throughout the study: orgasm function, libido, and satisfaction with overall sexual functioning. Depression was also evaluated at each visit. RESULTS: All patients reported orgasm delay and/or failure at the time of fluoxetine discontinuation. Orgasm function, libido, and satisfaction with sexual functioning improved during the 2-week fluoxetine washout period and during the bupropion treatment phase. Ninety-four percent of patients (29/31) had complete or partial resolution of their orgasm dysfunction at the end of bupropion treatment, and 81% of patients (25/31) were "much" or "very much" more satisfied with their overall sexual functioning. Most patients entered the study with decreased libido on fluoxetine. Libido was "much" or "very much" increased for 81% of patients (25/31) at the end of the study. In addition, depression scores on the Hamilton Rating Scale for Depression and Clinical Global Impressions-Severity scale significantly improved during the bupropion treatment phase. Finally, bupropion was well tolerated by most patients. CONCLUSION: Bupropion may be an appropriate antidepressant for patients who develop sexual dysfunction during fluoxetine treatment or for whom sexual dysfunction is a concern.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8276736&dopt=Abstract
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Neuropharmacology. 1983 Jul;22(7):927-9.
Daily bupropion injections for 3 weeks attenuate the NE stimulation of adenylate cyclase and the number of beta-adrenergic recognition sites in rat frontal cortex.
Gandolfi O, Barbaccia ML, Chuang DM, Costa E.
In rats receiving daily doses (50 mg/kg i.p. twice daily) of bupropion HCI (WellbutrinR) repeated for 21 days the Bmax of the beta-adrenergic receptor recognition sites located in the frontal cortex is reduced. This decrease is not associated with a decrease of the apparent affinity of these recognition sites. However the Vmax of the cAMP (cyclic AMP) generating system stimulated by NE is reduced suggesting that similarly to other antidepressants bupropion down regulates beta-adrenergic receptors located in the frontal cortex. Bupropion neither inhibits MAO (monoamine oxidase) nor releases biogenic amines but only weakly inhibits monoamine uptake in vitro.
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Psychopharmacology (Berl). 1989;99(1):122-8.
Strain-specific effects of antidepressants on escape deficits induced by inescapable shock.
Shanks N, Anisman H.
Department of Psychology, Carleton University, Ottawa, Ontario, Canada.
The effects of several antidepressants (desmethylimipramine, amitriptyline and bupropion) on escape deficits induced by inescapable shock were assessed in four strains of mice. The extent of the escape interference engendered by inescapable shock varied across strains of mice. These deficits of escape performance were differentially affected by the drug treatments across strains. Repeated administration of desmethylimipramine eliminated the escape interference in A/J, but did not affect the performance in Balb/cByJ, C57BL/6J or CD-1 mice. Bupropion, in contrast, had a modest effect only in CD-1 mice. Unlike these compounds, the 5-HT reuptake blocker, amitriptyline, was found to influence escape performance irrespective of whether the drug was acutely or chronically applied. It is suggested that (a) the relative contributions of various mechanisms subserving the escape interference may vary across strains of mice, hence accounting for the strain-specific effects of the drug treatments, and (b) various antidepressants influence performance by affecting different components of the behavioral output, some of which may be apparent after acute treatment while others are expressed only after repeated treatment with the compound.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2506597&dopt=Abstract
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