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Seretonin(Spelling?) reuptake inhibitors With MDMA

MiPt

Bluelighter
Joined
Dec 1, 2004
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2
Location
Texas
Sorry if someone has already asked this question, OK.... From what I know about the effects of seretonin reuptake inhibitors such as prozac, is that it causes seretonin to stay in your brain much longer than normal, and the neuron responsible for abosorbing it is blocked off. I was wondering if someone took prozac for enough time to get the full effect, and then Took ecstasy, What exactly would happen in your brain? I dont know for shure, but it sounds like your brain would be flooded with seritonin and have
no way to reabsorb it. ive asked my friend who has a PHD in BioChemisty and he said that it would indeed increase your high. But it would cuase your brain to make some kind of protien that would break down the seritonin and it would permentanly make you rely on antidepressents to keep your moods normal. If anybody has any Idea about this at all it would be much aprecciated.
 
People taking SSRIs are generally unable to get any effects for ecstacy...so I think you're wrong in your assumption that Prozac + E would increase your high; in fact, it does just the opposite. Although, I can't provide you with scientific reasoning as to why this is so. I understand your hypothesis: Prozac prevents serotonin reuptake and E releases more serotonin and therefore you'd assume that you'd just be flooded with serotonin - and have a better high. I'm not sure why this is not the case and I also wonder if this combination would make one very susceptible to serotonin syndrome.
 
I think the SSRI+MDMA=no trip idea only applies to regular users of SSRI's because regular users of SSRI's are used to a higher level of serotonin in their brain and when the MDMA tried to increase it - the effects are not noticeable. (I have no idea, just a bit of inferring :P).

Maybe if someone pre-loaded (someone that wasn't a regular SSRI user) with an SSRI it may increase your trip. (also increase the probability of encountering difficulties).

Maybe someone who knows what they're on about can help me out here :)
 
EpicureanDream, I agree that regular SSRI users don't get effects from ecstacy...but I'd also guess that preloading would reduce, not increase, the effects. I would assume the reason for this is the same as the reason why daily SSRI users don't get high (although I'm at a loss to give that reason). I have heard post-loading with SSRIs can help with the after effects (short term, ecstacy related depression) by increasing available serotonin.
 
Go combine an MAOI with ecstacy and tell me about it (if you live to tell me about it that is).

Combing an SSRI with cocaine prolonged the effects of cocaine up to 3 hours, when normally effects would last no more than 30 minutes.
 
Should be noted it was a double dose of prozac and it the user was not a user of SSRI's.
 
Go combine an MAOI with ecstacy and tell me about it (if you live to tell me about it that is).

Combing an SSRI with cocaine prolonged the effects of cocaine up to 3 hours, when normally effects would last no more than 30 minutes.

What does this have to do with the topic at hand? Cocaine isn't MDMA and a MAOI isn't a SSRI.
 
The reason is because MDMA releases serotonin through the reuptake transportor. Amphetamines (and MDMA) cause reuptake pumps to work in reverse. This is why you get the increased serotonin in the synapse. By taking a reuptake inhibitor, and jamming up the pumps, you are blocking the way that MDMA works.

peace,
beta theory
 
beta theory, you mentioned amphetamines...are you suggesting that SSRIs users will have lessened (or no) effects from amphetamines? I have personal experience with being on several different SSRIs and using Dexedrine and still getting "normal" effects. I was using the Dexedrine for some long study nights to finish papers, study, etc. and it definitely worked...just thought I'd note that I wasn't using it recreationally (or in recreational doses).
 
It is my understanding that the effects achieved from amphetamines are cause predominately by a large release of dopamine. Serotonin is released due to taking amphetamines, but is quite small in comparison to the release of dopamine. This is why you are still able to get good effects from amphetamines. Hope that clears it up.

peace,
beta theory
 
Amphetamines and MD-amphetamines (MDMA, MDA and MDE) are two different classes of drugs, with SSRIs preventing the effects of the latter ecstasy type drugs while not interfering with the stimulatory effects of the former type of drug. Classical amphetamines are primarily catecholamine (DA, dopamine, and NE, norepinephrine) releasers, while ecstasy is primarily a serotonin (5-HT) releaser. The DA/NE releasing effect is more addictive than the 5-HT releasing effect. However, MDMA also increase intracellular DA levels to some extent, which gives it some rewarding properties. MBDB, BDB, and MDAI (2-amino-5,6-methylenedioxyindan) are also serotonin releasers--but not dopamine releasers--and are not as widely abused as MDMA, nor are they self-administered by test animals. Interestingly, people can get high on the classical amphetamines for years without developing much long term tolerance, which is certainly not the case for MDMA users.

I have found that using cocaine while rolling on ecstasy destroys my ecstasy high, but YMMV. I have never heard of someone taking cocaine and ecstasy at the same time and lengthening their high that way, but there's a first time for everything I guess.

Over the long term, the use of SSRIs such as Prozac and Zoloft may increase available brain serotonin (5-HT), but the brain seems to compensate for this by actually reducing the available levels of dopamine (DA) in your brain. This neurochemical side effect is why many SSRIs can cause blunting of affect (that is, flattening of mood), and why they suck so much / have no recreational value. I have read that DA reuptake inhibitor type antidepressant drugs are currently being synthesized and tested, but I have my doubts as to whether they will be much better than the SSRIs.

Big pharma is also looking at acetylcholine nicotinic receptor agonists as a treatment for depression. One promising molecular candidate, ABT-594, is a nicotinic agonist that is reportedly 200x stronger than morphine at relieving pain, although ABT-594 is not thought to be an opioid, as its effects in rats are not reversed by the injection of naloxone, an opioid antagonist used for heroin overdoses. Whether ABT-594 will turn out to be an addictive drug of abuse is a question that is still up in the air at this point. It too releases NE and DA, so my bet is yes on that point.

In children at least, SSRIs have been shown only about 10 percent more effective than a sugar pill (a placebo) in alleviating depression. SSRIs have no recreational value and, in my opinion, are highly doubtful to be efficacious in the treatment of depression, for me at least. They are the modern day psychopharmacological snake oil. Marijuana, which reduces the release of corticotropin releasing factor (CRF), a stress hormone and is also a DA agonist, is a better antidepressant in my opinion, although its increase in susceptibility to psychotic disorders should be watched for and treated with atypical antipsychotics if necessary.
 
Lets see: MDMA-induced high is blocked in both chronic and acute users of SSRIs. As beta theory basically said. MDMA and other amphetamine cause release of monoamines by entering the cell through a monoamine transporter, and by an ionic cascade leads to reverse transport of monoamines. SSRIs (and other monoamine transporter blockers (coke, venlafaxine)) block this, by blocking amphetamine enterance.

The only difference between amphetamines is the affinity they have for dopamine, serotonin and noradrenaline transporters, which of course dictates which cells they enter and cause reverse transport in.

MDMAs pure action is actaully about equal serotonin/norandrenaline, but probably because of some 5-HT2A receptor indrect action in the prefrontal cortex, dopamine gets significantly released there. (There aren't many dopamine transporters in the prefrontal cortex anyway so amphetamines can't release dopamine directly there)
 
Thank you guys very much..... I going to take organic chem next summester so i hope i understand what you are talking about a little beter, but anyone could get the basic idea from your explanations.
Thank for the info
 
mdma and effexor

it was possible to get the affects of e while on a pretty high dose of effexor xr 300 mg/day....now the e did work better if one spaced the e as far from the effexor as possible...
this does cause its own troubles since many people on such doses of effexor can start to "miss" their effexor once the dose is about 12 hours late. And try to explain why u are carrying your effexor bottle with u to a club in NYC!!!!
And yes, more e is needed to go to the same state compared to a person not on effexor.
The same held true for paxil....except that paxil was a less effective anti depressant...and caused severely delayed ejaculation....which prompted a switch to effexor.....and a much happier camper =D =D
 
phishy2, I think one reason it is adviced not to take SSRIs + ecstacy is due to possibly serotonin syndrome...though I'm not positive.

Since amphetamines mostly act on DA and NA, would an SNRI + SDRI (selective norepinephrine and dopamine reuptake inhibitors) cause a decrease in the effects of amphetamines?

Say if someone was taking Cymbalta (a relatively new A/D that inhibits reuptake of both serotonin and norepinephrine fairly equally, as opposed to Effexor which has a significantly stronger effect on serotonin) and Wellbutrin (inhibits reuptake of dopamine), would this reduce the effects of amphetamines?
 
serotonin syndrome isn't likely, though it might be possible if someone took a massive dose of MDMA... the reason is because it's probably not that effective in blocking any possible neurotoxicity, and people shouldn't be encouraged to take prescription drugs in such a light-hearted manner, (side effects, idiopathic reactions, who knows).
 
serotonin syndrome usual requires there to be a monoamine oxidase inhibitor around to happen....such as syrian rue....or certain anti depressants....but people on such meds know...they have to avoid certain foods.

effexor and monoamine oxidase inhibitors is a big NO-NO!!!

i've just been hearing a lot saying that e does not work id u are on ssri's or effexor...but i'm just saying that it can especially with some moving around of the ssri dose times

now does the combination of effexor and e greatly increase the toxicity of e??

if it was a great increase in toxicity...i think it would have been figured out....if its subtle...no

and i treasure all those little holes in my brain...they took lots of work to have inserted in just the right places
8o 8(
 
how about effexor and 5-htp? what are the chances of serotonin syndrome by mixing those? and, also, if there is, at what dosages of 5-htp does serotonin syndrome become a risk, assuming the person was on a high dosage of effexor (300 mgs)?
 
Its quite possible, venlafaxine is probably the antidepressant with the largest history of serotonin syndrome effects, because it puts quite a big blockade on SERT AND NET, blocking most of the transporter routes out for serotonin in the frontal cortex..

As far as dosages, I don't have a clue, but its generally a bad idea to take 5-HTP if you're on an antidepressant.
 
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