wellbutrin interaction with marijuana

I am a healthy 27 year old male who has been on 300mg of Wellbutrin SR and 75mg of Seroquel (at bedtime) for a few months now. Would there be major interactions with this prescription and a moderate amount of marijuana?

Probably not. THC actually has very few interactions with other drugs. As wellbutrin is active with dopamine and norepinephrine receptors, and THC with cannibinoid receptors, the two really have nothing to do with each other.

thank you this really helped

The combining any drug can result in serious and sometimes very fatal reactions. Keep in mind that Marijuana increases your heart rate and depending on the other drug taken with it can also increase your heart rate. Taken together it can cause arithmia, stroke, heart attack...etc. I would say consult your Dr. There is something called DR/Patient privilege that protects you so don't be stupid and take an anonymous person's comment on a message board...see your Dr.

Actually Wellbutrin could potentially interact with pot in that you could end up with even worse memory and cognition than you have just smoking pot.

D2 dopamine receptors enable Δ9-tetrahydrocannabinol induced memory impairment and reduction of hippocampal extracellular acetylcholine concentration
F Nava,1* G Carta,2 A M Battasi,1 and G L Gessa1,2
11Laboratory of Neuropsychopharmacology, Department of Neuroscience ‘B.B. Brodie', University of Cagliari, Cagliari, Italy
22Neuroscience S.c.a.r.l., Cagliari, Italy
*Author for correspondence: Email: lgessa@unice.it
Received September 15, 1999; Revised March 30, 2000; Accepted April 5, 2000.
Small right arrow pointing to: This article has been cited by other articles in PMC.

Abstract

* The systemic administration of Δ9-tetrahydrocannabinol (2.5–7.5 mg kg−1) reduced hippocampal extracellular acetylcholine concentration and impaired working memory in rats.
* Both effects were antagonized not only by the CB1 cannabinoid receptor antagonist SR141716A (0.5 mg kg−1, i.p.) but also unexpectedly by the D2 dopamine receptor antagonist S(−)-sulpiride (5, 10 and 25 mg kg−1, i.p.). Conversely, Δ9-tetrahydrocannabinol-induced memory impairment and inhibition of hippocampal extracellular acetylcholine concentration were potentiated by the subcutaneous administration of the D2 dopamine receptor agonist (−)-quinpirole (25 and 500 μg kg−1). The inhibition of hippocampal extracellular acetylcholine concentration and working memory produced by the combination of (−)-quinpirole and Δ9-tetrahydrocannabinol was suppressed by either SR141716A or S(−)-sulpiride.
* Our findings suggest that impairment of working memory and inhibition of hippocampal extracellular acetylcholine concentration are mediated by the concomitant activation of D2 dopamine and CB1 cannabinoid receptors, and that D2 dopamine receptor antagonists may be useful in the treatment of the cognitive deficits induced by marijuana.

Keywords: Δ9-Tetrahydrocannabinol, D2 dopamine receptors, working memory, acetylcholine

Physiological release of striatal acetylcholine in vivo: modulation by D1 and D2 dopamine receptor subtypes

P DeBoer and ED Abercrombie

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey, USA.

Our experiments assessed the modulation of striatal acetylcholine (ACh) output by dopamine (DA) receptor subtypes under physiological conditions using in vivo microdialysis in awake rats. The degree to which the dopaminergic modulation of striatal cholinergic neurons might vary as a function of local extracellular ACh level also was examined by application of varying concentrations of the acetylcholinesterase (AChE), inhibitor neostigmine (NEO) in the microdialysis perfusate. Under physiological conditions (O NEO), the amount of ACh in the dialysates was 25.1 +/- 2.2 fmol/20-microliters sample (n = 20) whereas values of 67.9 +/- 3.5 (n = 35) and 527.7 +/- 56.1 (n = 13) fmol/20- microliters sample were obtained when the applied NEO concentration was 10 and 100 nM, respectively. In the absence of NEO, a low dose of the indirect DA agonist amphetamine (AMPH; 2 mg/kg i.p.) failed to affect striatal ACh output; a higher AMPH dose (10 mg/kg i.p.) significantly decreased the amount of ACh in dialysates. Under physiological conditions, the direct D2-selective agonist quinpirole (3 mg/kg i.p.) decreased extracellular ACh in striatum to nondetectable levels and the direct D1-selective agonist SKF-38393 (10 mg/kg i.p.) produced a significant increase in this measure. Analysis of the changes in striatal ACh output produced by administration of these DA compounds in the absence vs. presence of local NEO revealed that 10 nM NEO did not qualitatively alter the pharmacological responsivity of this system as compared to the physiological condition. However, in the presence of 100 nM NEO, 2 mg/kg AMPH elicited a significant increase in striatal ACh output. At the 100 nM NEO concentration it also was observed that the amplitude of the quinpirole-induced inhibition of ACh efflux did not increase further in proportion to basal ACh levels whereas the amplitude of the increase in ACh output produced by SKF-38393 was linearly related to basal ACh levels across all NEO concentrations. Under conditions where cholinergic pharmacological responsivity was minimally affected (10 nM NEO), the D2 receptor antagonist haloperidol (1 mg/kg i.p.) increased striatal ACh output by 50% and the D1 receptor antagonist SCH-23390 (0.5 mg/kg i.p.) decreased this variable by 41%. Under these conditions, the inhibitory action of quinpirole on ACh output could be reversed by subsequent administration of AMPH (5 mg/kg i.p.) and this effect of AMPH could then be blocked by administration of SCH-23390. Thus, under physiological or low NEO (10 nM) conditions a prevalent D2-mediated inhibition as well as an opposing D1-mediated excitation of striatal ACh output can be demonstrated. At a higher NEO concentration (100 nM), regulation of the striatal ACh system by DA receptor subtypes is differentially affected such that the D2-mediated inhibitory influence no longer predominates over the D1-mediated excitatory drive. Caution should be exercised when interpreting ACh efflux data obtained using microdialysis under conditions of AChE inhibition.
Volume 277, Issue 2, pp. 775-783, 05/01/1996
Copyright © 1996 by American Society for Pharmacology and Experimental Therapeutics

As you are well aware Wellbutrin is a NDRI - an Noradrenaline/Dopamine Reuptake inhibitor. Thusly Wellbutrin will stimulate or act as an agonist at dopamine D2 receptors. Depending on how things are balanced out in your brain the combination of the two could really screw you up.

THC is one of the active ingredients in pot.

And witness:

Bupropion SR (Wellbutrin/Zyban) worsens mood during marijuana withdrawal in humans.

Haney M, Ward AS, Comer SD, Hart CL, Foltin RW, Fischman MW.

Division on Substance Abuse, New York State Psychiatric Institute, College of Physicians and Surgeons of Columbia University, New York 10032, USA. mh235@columbia.edu

RATIONALE: Symptoms of withdrawal after daily marijuana smoking include increased ratings of irritability and depression. Similar mood symptoms are reported by cigarette smokers during nicotine abstinence. OBJECTIVE: Given the successful use of sustained-release bupropion in treating nicotine dependence, this study investigated how maintenance on bupropion influenced symptoms of marijuana withdrawal compared to maintenance on placebo. METHODS: Marijuana smokers (n=10) were maintained outpatient on active (300 mg/day) or placebo (0 mg/day) bupropion for 11 days, and were then maintained inpatient on the same bupropion dose for 17 days. For the first 4 inpatient days, participants smoked active marijuana [2.8% delta9-tetrahydrocannabinol (THC)] 5 times/day. For the remaining inpatient days, participants smoked placebo marijuana (0.0% THC) 5 times/day. Participants were then maintained outpatient on the alternate dose of bupropion for 11 days, followed by a second inpatient residential stay, paralleling the first. Medication administration was double-blind. Mood, psychomotor task performance, food intake, and sleep were measured daily during each inpatient phase. The order of active and placebo bupropion maintenance was counterbalanced between groups. RESULTS: Bupropion had few behavioral effects when participants smoked active marijuana. During placebo marijuana smoking, i.e., active marijuana withdrawal, ratings of irritability, restlessness, depression, and trouble sleeping were increased by bupropion compared to placebo maintenance. CONCLUSIONS: These data suggest that bupropion does not show promise as a potential treatment medication for marijuana dependence.

Publication Types:

* Clinical Trial
* Randomized Controlled Trial
* Research Support, Non-U.S. Gov't
* Research Support, U.S. Gov't, P.H.S.


PMID: 11401006 [PubMed - indexed for MEDLINE]

To summarize - Wellbutrin + Pot = Potentially bad mojo.

I smoke weed everyday with Wellbutrin XL 300mg. And everything is straight. Just when you do smoke for the first time on it, take smaller hits because it comes on fast, but once you get used to it you can toke like normal. May feel really detached and dissociated the first time, and sweat a lot, but that will go away. So toke safely, and you'll be fine.

I was told by a psychiatrist that when you smoke pot while on Welbutrin it pretty much cancels out the effects that this drug is suppose to help you with. So if it is depression or whatever else it might be by smoking pot with it is like not taking the Welbutrin in the first place.

"RESULTS: Bupropion had few behavioral effects when participants smoked active marijuana."

im really questioning how much you know about what you posted.

I smoke everyday and take Wellbutrin with no problems at all

Would moderate intake of marijuana either negate or reduce the effects of an antibiotic like Vancomycin? The pot calms my nerves and helps me forget that the Vancomycin costs almost as much per month as a new Kia.



Thanks.