Drugs online research references
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 357% for the combination) and in the Acb (224% vs 645%). The bupropion-induced NE increases were potentiated by fluoxetine mainly in the Ht. Bupropion did not significantly affect the extracellular 5-HT concentrations in all the 3 brain areas tested. In summary, the present study demonstrated that bupropion can increase extracellular DA and NE concentrations in several mesocorticolimbic areas, which may have an impact on bupropion's antidepressant actions. Furthermore, fluoxetine can potentiate the bupropion-induced DA and NE increases, which may produce more effective and rapid antidepressant actions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11804614&dopt=Abstract
word match zyban online literature
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 significant anxiolytic activity. There was no difference in the activating effects between the 2 antidepressants. Selection between these 2 agents cannot be based on either anticipation of differential anxiolytic activity or differential CNS side effect profiles.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11816866&dopt=Abstract
word match zyban online literature
Prescrire Int. 2001 Dec;10(56):163-7.
Amfebutamone/bupropion for smoking cessation: new preparation. Nicotine replacement therapy is safer.
[No authors listed]
(1) For smokers who want to quit and who qualify for pharmacological support, the various forms of nicotine replacement therapy available in France yield a one-year cessation rate of about 14-18%, compared to about 10% with placebo. (2) Amfebutamone (also known as bupropion) is structurally related to an amphetamine psychostimulant. (3) The clinical file mainly contains data from a dose-finding study, two placebo-controlled trials, and a trial comparing amfebutamone + transdermal nicotine with amfebutamone + transdermal placebo. (4) It has not yet been shown that the approved dose regimen of 300 mg/day is more effective than 150 mg/day, or that the treatment period of 7-9 weeks is optimal. (5) Compared to placebo, the one-year cessation rate was only about 13% higher (absolute value) in one trial, much less in the dose-finding study (3%), and not determined in the other two trials. The trial comparing amfebutamone with nicotine suffers from too many methodological weaknesses to show any difference in the efficacy of the two drugs. There has been no specific assessment of amfebutamone in patients with coronary heart disease. (6) There is no basis for combining amfebutamone with nicotine replacement therapy, as there is no evidence of higher efficacy. Furthermore, cardiovascular risk may be increased. (7) Amfebutamone can have serious adverse effects: the estimated risk is approximately 0.1% for convulsions and 3% for potentially severe hypersensitivity reactions. The adverse effects seem to be similar to those of appetite-suppressant amphetamines, including insomnia, weight loss and hypertension. The possible risk of heart valve disease has not been ruled out, because echocardiographic follow-up studies have not been done. (8) Potential adverse effects and drug interactions should contraindicate the use of amfebutamone by patients with a history of cardiovascular, neurological or psychiatric disorders. (9) In practice, when someone needs drug support to quit smoking, nicotine replacement therapy should be tried first.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11824437&dopt=Abstract
word match zyban online literature
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Antibiotics and prescription medications online literature ||