Drugs online research references
Adv Biochem Psychopharmacol. 1982;31:277-86.
Neurochemical and neuropharmacological investigations into the mechanisms of action of bupropion . HCl--a new atypical antidepressant agent.
Ferris RM, Maxwell RA, Cooper BR, Soroko FE.
In the present study, bupropion has been shown to be effective in several behavioral models predictive of antidepressant activity suggesting that it should be an effective antidepressant in man. Furthermore, the data also show that the antidepressant activity of the drug cannot be due to its ability to inhibit MAO present in brain or to increase the release of biogenic amines from nerve endings. It also appears unlikely that the weak properties of the drug as an inhibitor of catecholaminergic pumps in brain csn explain its antidepressant activity. However, the weak but selective block of dopaminergic pumps observed in vivo can be correlated with the mild CNS stimulant properties observed in rodents. Bupropion, failed to desensitize beta-adrenergic receptors in rat cerebral cortex in chronic studies and exhibited equivocal results in acute studies. These neurochemical properties of bupropion serve to distinguish it from typical antidepressants of the MAOI and tricyclic classes and suggest that it should be classified as an atypical antidepressant, whose mechanism of action must still be elucidated.
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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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Neuropharmacology. 1983 Nov;22(11):1257-67.
Bupropion: a new antidepressant drug, the mechanism of action of which is not associated with down-regulation of postsynaptic beta-adrenergic, serotonergic (5-HT2), alpha 2-adrenergic, imipramine and dopaminergic receptors in brain.
Ferris RM, Beaman OJ.
The present experiments were undertaken to determine: (1) whether bupropion had any direct effects on receptors present in rat brain; (2) whether the drug could down-regulate postsynaptic beta-adrenergic, alpha 2-adrenergic, serotonergic, imipramine and dopaminergic receptors after chronic administration, as had been demonstrated for tricyclic antidepressants, monoamine oxidase (MAO) inhibitors, electroconvulsive therapy (ECT) and "atypical" antidepressants. Bupropion was found to be weak or inactive when its affinity for 14 different receptors present in brain was assessed by binding assays. The drug failed to desensitize beta-adrenergic receptors in the cerebral cortex of the rat as determined by [3H]dihydroalprenolol binding, after being administered at 25 mg/kg (i.p.) once a day for 6 weeks, or after being administered by the intraperitoneal route to rats at doses as large as 150 mg/kg per day for 4 days. When administered at doses of 37.5, 75 and 150 mg/kg per day for 21 days, the drug had no effect on beta-adrenergic, alpha 2-adrenergic, imipramine or serotonergic (5-HT2) receptors in the brain of the rat as determined by Scatchard analysis of the binding data. These data show that the antidepressant activity of bupropion is not associated with a down-regulation of receptors in the CNS commonly implicated in the mechanism of action of antidepressant drugs. Bupropion also produced a dose-dependent tendency to decrease the activity of norepinephrine-stimulated adenylate cyclase in slices of cerebral cortex obtained from rats treated chronically with the drug. However, the decrease was highly variable, was most obvious in tissues obtained from rats receiving large, non-pharmacologically relevant doses (150 mg/kg per day) of the drug and was statistically significant at only one of three concentrations of the agonist that produced maximal stimulation of the enzyme.
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