Posted by Chairman_MAO on February 16, 2004, at 12:33:33
In reply to Wellbutrin fast acting or build up?, posted by action on February 16, 2004, at 7:41:43
Wellbutrin undergoes extensive metabolism, and its three active metabolites accumulate over time. As this accumulation takes place, the effect becomes more robust. The "antidepressant" effect takes place after at least a month of chronic treatment, like all antidepressants--except "classic" stimulants and opioids, heh.
In regard to its effect on dopamine, I believe the jury is still out. From a psychopharmacological perspective, it probably has SOME weak dopaminergic effects, direct or indirect, given that it makes some people horny, can induce hallucinations, and because some people report muscle twitches that are much like those reported with dopaminergic agents. The study below shows that chronic administration produces a blockade of the dopamine uptake transporter of 26%--a value I am not sure means much at all. Anyone else care to comment on this?
Honestly, I've learned that from a clinial perspective, whether it has any effect on doapmine or not is really not relevant; just pay attention to whether it works or not. :)IMHO, Wellbutrin is simply a stimulant weak enough to evade scheduling (that means WEAK). It is structurally similar to the diet drug diethylpropion and the illegal drug cathinone. Draw your own conclusions.
Provigil has been shown completely ineffective for ADD. Wellbutrin has spotty efficacy, but better than Provigil. If you want energy, Provigil is better.
I started Wellbutrin for ADD because, due to my history, no doctor--except a private one--would ever give me amphetamine, which is the only thing that helps worth a damn. Thusfar I notice no beneficial effects, though I am only at 150mg of the XL. I am not optimistic. Let me know how your journey goes!
Biol Psychiatry. 2003 Oct 15;54(8):800-5.
In vivo activity of bupropion at the human dopamine transporter as measured by positron emission tomography.Learned-Coughlin SM, Bergstrom M, Savitcheva I, Ascher J, Schmith VD, Langstrom B.
GlaxoSmithKline, Five Moore Drive, Research Triangle Park, NC 27709, USA.
BACKGROUND: Converging lines of evidence are consistent with an inhibitory effect of the antidepressant and smoking-cessation aid bupropion on dopamine and norepinephrine reuptake, but the in vivo effects of the drug at the human dopamine transporter (DAT) have not been studied to date. This study employed positron emission tomography (PET) to assess the extent and duration of DAT receptor occupancy by bupropion and its metabolites under conditions of steady-state oral dosing with bupropion sustained-release (SR) in healthy volunteers. METHODS: Six healthy male volunteers received bupropion SR 150 mg daily on days 1 through 3 and 150 mg every 12 hours on day 4 through the morning of day 11. PET investigations were performed between 1 and 7 days before initiation of bupropion SR dosing, as well as 3, 12, and 24 hours after the last dose of bupropion SR on day 11. RESULTS: Bupropion and its metabolites inhibited striatal uptake of the selective DAT-binding radioligand (11)C-betaCIT-FE in vivo. Three hours after the last dose of bupropion SR, average DAT occupancy by bupropion and its metabolites was 26%-a level that was maintained through the last PET assessment at 24 hours after dosing. CONCLUSIONS: Bupropion and its metabolites induced a low occupancy of the striatal DAT over 24 hours under conditions of steady-state oral dosing with therapeutic doses of bupropion SR. These data are consistent with the hypothesis that dopamine reuptake inhibition may be responsible in part for the therapeutic effects of the drug.
poster:Chairman_MAO
thread:313435
URL: http://www.dr-bob.org/babble/20040215/msgs/314085.html