Drugs online research references
J Clin Psychiatry. 1998 Mar;59(3):112-5.
Bupropion as an antidote for serotonin reuptake inhibitor-induced sexual dysfunction.
Ashton AK, Rosen RC.
State University of New York at Buffalo, School of Medicine, USA.
BACKGROUND: Serotonin reuptake inhibiting antidepressants (SRIs) are reported to cause sexual dysfunctions, including reduction in desire, arousal, and orgasm. This study evaluates the efficacy of bupropion in ameliorating sexual dysfunctions in patients receiving SRIs. METHOD: Forty-seven patients in an outpatient psychiatric practice who complained of SRI-induced sexual dysfunction accepted a trial of bupropion as an adjunct to their SRI, either as a p.r.n. or as a fixed-dose scheduled medicine. Patients received 75 mg or 150 mg of bupropion 1 to 2 hours before sexual activity. If this was insufficient to reduce their complaints, dose was increased gradually to 75 mg t.i.d. and sustained for 2 weeks. This regimen was then continued if successful. RESULTS: Bupropion successfully reversed a variety of sexual dysfunctions caused by SRIs in 31 (66%) of 47 patients. Fifty-two (69%) of 75 sexual complaints improved with bupropion treatment. The p.r.n. use of bupropion assisted 18 (38%) of 47 patients. Side effects of anxiety and tremor led to discontinuation of bupropion in 7 (15%) of 47 patients. Otherwise, bupropion was well tolerated. CONCLUSION: Bupropion administration may be a safe and effective method of treating SRI-induced sexual dysfunction. Placebo-controlled, double-blind studies are needed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9541153&dopt=Abstract
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J Pharmacol Exp Ther. 1999 Jan;288(1):88-92.
Noncompetitive functional inhibition at diverse, human nicotinic acetylcholine receptor subtypes by bupropion, phencyclidine, and ibogaine.
Fryer JD, Lukas RJ.
Division of Neurobiology, Barrow Neurological Institute, Phoenix, Arizona, USA.
Nicotinic acetylcholine receptors (nAChR) are diverse members of the neurotransmitter-gated ion channel superfamily and play critical roles in chemical signaling throughout the nervous system. The present study establishes the acute functional effects of bupropion, phencyclidine, and ibogaine on two human nAChR subtypes. Function of muscle-type nAChR (alpha1 beta gamma delta) in TE671/RD cells or of ganglionic nAChR (alpha3 beta4 alpha5+/-beta2) in SH-SY5Y neuroblastoma cells was measured with 86Rb+ efflux assays. Functional blockade of human muscle-type and ganglionic nAChR is produced by each of the drugs in the low to intermediate micromolar range. Functional blockade is insurmountable by increasing agonist concentrations in TE671/RD and SH-SY5Y cells for each of these drugs, suggesting noncompetitive inhibition of nAChR function. Based on these findings, we hypothesize that nAChR are targets of diverse substances of abuse and agents used in antiaddiction/smoking cessation strategies. We also hypothesize that nAChR play heretofore underappreciated roles in depression and as targets for clinically useful antidepressants.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9862757&dopt=Abstract
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J Clin Psychiatry. 1983 May;44(5 Pt 2):60-2.
Preclinical toxicology of bupropion: an overview.
Tucker WE Jr.
In preclinical studies, the toxicologic profile of bupropion was determined in laboratory animals using exaggerated doses of drug in a variety of toxicologic assays. Under overdose conditions, clinical signs primarily referable to the central nervous system were seen in rats, mice, rabbits, and dogs. Very mild, reversible hepatotoxicity and anemia occurred in dogs with chronic dosing; lifetime administration in rats caused hepatocellular hypertrophy and focal hepatic hyperplasia. In both rats and dogs, there was an increase in liver weight related to hepatic enzyme induction. Appropriate tests indicated that bupropion is unlikely to have the potential to cause teratogenic, mutagenic, or carcinogenic effects in man.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6406465&dopt=Abstract
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