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Bupropion appears to enhance monoaminergic neurotransmission via its effects on both the NE and DA transporterswith subsequent reuptake inhibition of these 2 neurotransmittersBupropion and 2 of its metaboliteshydroxybupropion and threohydrobupropionwere shown to decrease the uptake of NE and DA into rat and mouse synaptosomes9 Bupropion’s activity as a DA transporter inhibitor is further supported by a recent study showing approximately a 3-fold increase in expression of the immediate early gene c-fos in human DA transporter cellsandif coincubated with DAan attenuation of the DA-induced c-fos in human DA transporter cells14 Acute administration of bupropion reduces firing of brain stem NE and DA neuronsdata on fileGlaxoSmithKlineResearch Triangle ParkN.CAdditionallyfiring rates of NE neurons in the locus ceruleus are inhibited after acute bupropion administration9 Microdialysis studies following acute administration of bupropion demonstrate that extra-cellular NE and DA concentrations are increased in the nucleus accumbensdata on fileGlaxoSmithKlineResearch Triangle ParkN.CFurther evidence of the NDRI action of bupropion was found when administration of NEor DA-blocking drugs was shown to reduce the efficacy of bupropionand hydroxybupropionin animal models of depression15.
Plots of the steady-state plasma concentrations of bupropion over a 24-hour period for the IRSRand XL formulations of bupropion are presented in Figure 1data on fileGlaxoSmithKlineResearch Triangle ParkN.CWith steady-state dosing at 300 mg/dayboth the SR and XL formulationsrelative to the IR formulationdeliver an equivalent amount of bupropionAUCand do so while producing C max similar to or somewhat less than those seen with the IR formulationSince some adverse events are believed to be associated with C maxit is worth noting that the SR and XL formulations decrease the number of daily exposures of peak plasma levels to twice and once dailyrespectivelyImportantlytime to C maxT maxis prolonged with the SR3 hoursand XL formulations5 hoursrelative to the IR formulation2 hoursBoth the prolongation of T max and the decrease in the number of peak plasma levels may result in better tolerabilityalthough this has not been formally evaluatedWith once-daily dosing of the XL formulation in the morningplasma bupropion concentration levels are lower during evening hours compared to the SR formulationFigure 2data on fileGlaxoSmithKlineResearch Triangle ParkN.CThis may result in a lower rate of insomniaan adverse event that has been reported to be correlated with plasma concentrations5 The extended release of bupropion seen with the XL formulation is achieved by a moisture-barrier coating and a control-releasing coating surrounding a tablet core containing bupropionThe integrity of the delivery matrix is essential to providing an extended-release ratechewingcuttingor crushing bupropion XL tablets would disrupt the delivery matrixresulting in immediate release of bupropionwhich could cause significant adverse events.
The development of bupropion resulted from a targeted program designed to produce an antidepressant with a unique pharmacologic profile that offered safety and tolerability advantages over existing agents1 Bupropion’s safety and efficacy were established in several clinical trialsand with U.SFood and Drug AdministrationFDAapproval in 1989it was introduced as a treatment for major depressive disorderThe formulation was an IR tabletwhich required thrice-daily dosingAlthough clinically effectivethe dosing schedule was inconvenient for patientsBecause of this inconvenienceas well as evidence implicating a relationship between peak plasma concentrations and some adverse eventsdevelopment of an SR formulation was initiated45.
Two cases of elderly patients falling backwards have been attributed to the effects of bupropion on the basal gangliaRef]
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