wellbutrin interaction with 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: _[removed]_ 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. _[removed]_ 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.

I started smokin weed bout a week ago, I go slow since I just started smokin it, and I take wellbutrin and I don't feel any interaction with it.... On the other hand feels good and relax with weed, so gonna increase my weed consumption...

I think you can smoke pot while on bupropione but be cautious. Don't try to push anything. I did it for two days in a row ending yesterday. I also drank five or six alcoholic beverages while smoking about half a joint. I drank the drinks over many hours. There were no extreme adverse effects. But I must admit, the combination made me feel and act quite a bit dumber than usual. I mean I am not a regular smoker of pot. I drink fairly regularly. Smoking some high grade pot after a long period of abstinence resulted probably in a stronger effect than if I smoked pot daily. Combining it with alcohol and zyban seemed to increase the sort of dumbing down effect of pot. I usually don't feel so childishly dumb when I drink, but pot sort of deactivates my ability to think linearly, and also messes with my ability to concentrate on linear activities. I can, of course, really get into or a open-ended conversation of an imaginative variety -- like talking about flights of ideas or stories. But rules and math seem hard to comprehend on pot. I notice this was very apparent while on zyban. So if you decide to smoke pot and take zyban, from my experience, it may accentuate that spaced out feeling pot causes. You might be better off smoking pot and relaxing in a park or on the beach, then hanging out with friends playing board games or trying to do some work. But that is usually the case anyway. It is hard to say though whether it was the zyban or the combination of alcohol and pot that resulted in my sort of spaced out, childish dumbness. Don't get me wrong. Sometimes that state can be a nice change! I know that sounds weird but it's true.

For me I'm going to try to slow down, reduce, and possibly avoid ingesting alcohol and pot while on zyban though. You can tell pot and alcohol feel different while on zyban. There is a definite synergistic effect. The worse thing you cold do is chug alot of alcohol and do bong rips like some hippie frat boy If you're that kind of drinker and smoker, I would either make a concerted effort to avoid that behavior, or just stay away from it until you're off the zyban. I think if you maybe drank two drinks over two hours every other night it would be ok, or if you smoked maybe a few tokes at night you should be fine. But don't blame me if you have a psychotic fit. If you're taking zyban for depression and you ingest a hallucinogen like pot, you could have a psychotic reaction. I mean you could have one even without zyban, and zyban is known to sometimes result in psychosis.

I am taking Wellbutrin and i must say, while smokeing weed on this antidepressant, my heart rate was way up, pounding in my chest, just thinking about this makes your heart rate go up even more, like a panic attack. The best thing to do is not check your heart rate in the first place if you mix the two together. Im not sure if it was because i havent smoked in a long time or if it was really strong budz or if it was the combination of my antidepressants with weed, but i freaked out.. i thought God was sending me signs... on the TV, out of my own mouth, out of other peoples mouths without them even knowing it, it was insane. I have has Phycosis and was locked in a ward for a week. Not sure if it was the weed, cain, dxm, or what, but im saying be careful man. If you ever feel like you dont know what reality really is, you should get help asap.

I've smoked marijuana HEAVILY for many years. At least a half an ounce a week. Now that I'm on wellbutrin my memory turns to absolute sh*t. I mean like Horrible. Motivated me to quit smoking pot. Once I finish this Half ounce out this week I'm not buying again.

i exprienced grand mal seizures after smoking marijuana while taking wellbutrin XL 300mg. i know seizures are a very rare side effect of this medication and this rarely occurs with alcohol, so i was especially surprised when this happened to me smoking weed. i had a terrible high the night before, and when i smoked the next night, i seizured (on and off but frequently) for 2 hours. it's worth mentioning that i have never had a seizure before. so if you have a bad high, stop smoking weed! THC is lipid soluble and takes 3 months to leave your body so the levels get higher and higher in your body.