Evidence that the acute behavioral and electrophysiological effects of bupropion (Wellbutrin) are mediated by a noradrenergic mechanism. Down regulation of beta-receptors by bupropion and its major metabolite in mouse brain. Rx drugs

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Neuropsychopharmacology. 1994 Oct;11(2):133-41.
Evidence that the acute behavioral and electrophysiological effects of bupropion (Wellbutrin) are mediated by a noradrenergic mechanism.

Cooper BR, Wang CM, Cox RF, Norton R, Shea V, Ferris RM.

Division of Pharmacology Burroughs Wellcome Co., Research Triangle Park, North Carolina 27709.

Bupropion (BW 323U66) has been considered a dopaminergic antidepressant based on its ability to inhibit the uptake of dopamine (DA) somewhat more selectively than it inhibits uptake of norepinephrine (NE) or serotonin (5-HT). This report describes new evidence that bupropion selectively inhibits firing rates of NE cells in the locus coeruleus (LC) at doses significantly lower than those that inhibit activity of midbrain DA cells or dorsal raphe 5-HT cells. The IC50 dose (13 mg/kg i.p.) for inhibition of LC firing produced plasma concentrations that were not significantly different from those generated by the ED50 in the Porsolt test (10 mg/kg i.p.). The fourfold higher dose needed to inhibit DA cell firing (IC50 = 42 mg/kg i.p.) was similar to the dose associated with locomotor stimulation in freely moving rats. Bupropion did not change the firing rates of 5-HT cells in the dorsal raphe nucleus at any dose. In both in vitro and in vivo tests, the metabolite 306U73 (hydroxybupropion), a weak inhibitor of NE uptake, was approximately equipotent to bupropion with regard to inhibition of LC cells. Another metabolite, 494U73, had no effect on LC firing rates over a wide range of doses. Because of species variation in metabolism, 306U73 was not detected in plasma of rats after i.v. doses of bupropion that inhibited LC firing. Only trace amounts of 306U73 were detected after bupropion dosing for the Porsolt test. Pretreatment with reserpine markedly depleted catecholamines and reduced (by 30-fold) the potency of bupropion to inhibit LC firing.(ABSTRACT TRUNCATED AT 250 WORDS)

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OBJECTIVE: To investigate the toxicity of bupropion hydrochloride in deliberate self-poisoning in adults and accidental ingestion by children. DESIGN AND SETTING: Prospective study of cases identified from calls to the New South Wales Poisons Information Centre (NSW PIC), with follow-up through hospital medical records. PARTICIPANTS: Patients with bupropion poisoning managed in hospital, about whom the NSW PIC was contacted for advice, from 1 November 2000 to 31 July 2001 (59 adults and 10 children). MAIN OUTCOME MEASURES: Clinical effects, adverse outcomes (including seizures and death) and treatment. RESULTS: 45 of the 59 adults were followed up (76%), 19 of whom had taken bupropion alone. Major clinical effects of bupropion included sinus tachycardia (83%), hypertension (56%), seizures (37%), gastrointestinal symptoms (37%) and agitation (32%). Seizures were dose-dependent, with those having seizures ingesting a significantly higher median dose (P = 0.02). All seizures were brief and self-limiting. 29 patients received decontamination therapy. 10 patients required pharmacological sedation, 10 were admitted to intensive care and six were intubated. None died. Eight of 10 accidental ingestions by children were followed up (80%); one child had symptoms (vomiting and hallucinations). CONCLUSIONS: Bupropion overdose caused significant clinical effects in adults, but few in children.

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Neuropharmacology. 1986 Dec;25(12):1323-6.
Down regulation of beta-receptors by bupropion and its major metabolite in mouse brain.

Perumal AS, Smith TM, Suckow RF, Cooper TB.

Mice were treated with bupropion Compound II (major metabolite of bupropion) or desmethylimpramine (DMI) twice a day intraperitoneally for either 1 or 3 weeks. The binding of dihydroalprenolol and spiroperidol in the frontal cortex and limbic forebrain areas were analyzed. There was a significant reduction in beta-receptors in the frontal cortex induced by DMI at both times examined. Bupropion showed a significant reduction of beta-receptor in the frontal cortex by 3 weeks. Though propiophenone did not have any significant effect on beta-receptors in the frontal cortex, it down-regulated beta-receptors in the limbic forebrain area significantly by 1 and 3 weeks. There was no significant effect of buropion or propiophenone on the binding of spiroperidol either in the cortex (S2 receptor) or in the limbic forebrain (dopaminergic). These results show that bupropion may exert part of its clinical effect through its metabolite propiophenone.

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