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amphetamine mechanisim for blockade of cannabinoid mediated effects

allthegoodjwh's

Greenlighter
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Aug 8, 2012
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For a while now I've been trying to figure this out and all ive found out is that while it is know that this happens not a lot is know as to how it happens I mean in theory all amphetamine dose is increase dopamine norephinephrine and to an extent seratonin levals
I mean for an example amphetamine makes benzodiazepines less potent due to them being cns opposites in effect
But benzodiazepines seem to make weed less effective to even though technically they should increase potency (if amphetamine exerted its inhibiting effect on weed through it being a cms stimulant)


I know that synthetic cannabis has knew antagonist properties and would assume thc does to a lesser extent and amphetamine causes a ca+2 influx through that receptor and that's how it inhibits that receptor
I've also found that amphetamine litterally stops hallucinogens (for example psilocybin mushrooms) to the point I accuse them of being bunk untill I try them without it

It's weird it seems to cause the need for increased amounts of almost every drug due to shorter duration or decrease in potency expect of course other stimulants which it then synergizes with

One last thing maybe its due to it being a full agonist or just an increase in potency but I found that synthetic cannabinoids would magnify the effects of amphetamine (it would still wear off faster and have a faster growth of tolerance)
And lyrica (tryptophan and ghb properties or glutamate/other) would have a potentiating effect (I belive this to obviously be caused by something other than its gabaergic properties) anyways I was hoping some could shed some light on this advanced drug forum style
 
If there's a question in here I didn't find it. I've personally never experienced what you're describing with this combination, theoretically there's no reason amphetamine should block cannabis effects, and I don' think there's any support in the literature either.
 
Last I checked it might be a case of a generally excitatory drug mixed with a generally inhibitory drug. There is a lot more to that, especially when referring to individual regions in the brain, but is that what you wanted to know? We can go more in depth if need be.
 
Well cannabis works experientially as an amplifier and sedative; in my experience which was a long time ago - most of the sedative effects are overridden by speed and to some degree you just amplify the speed state.
As to psychedelics if your on a dopermineric rush this can to some degree dominate over what's going on at the serotonergic sites
 
Well to rephrase the main effect that I would be reffering to would be the psychadellic headspace I get from smoking large doses of weed
Basically a mixture of basically making everything look more beautiful and a dissociative body feeling I found this to either only happen for a high doses of amphetamine not at all
It's marijuana and then secondly psychadellics they seem to either wear off much faster or barley work at all
I started this forum because I wondered if someone knew the mechanisim amphetamine exerted to do this
I assume if not fully then partially to blame are altered levals of monoamines

There was another forum on bluelight in which various people mentioned that while on meth (my question is really about dextroamphetamine but they're very simmilar) they found thay marijuana barley worked or wore off way to fast in addition to that I have known numerous people who have noticed the same thing happen as well as myself I apologize if what I am saying is confusing
 
EA said:
We can go more in depth if need be.

I'd like to, 'cause I think I don't really understand it. The downstream effects of amphetamines and cannabinoids are complex and multifaceted. I don't know which circuits (and which mediating neurotransmitters) you'd look to to see the interaction. Do we have a physiological story more specific than general excitation vs. inhibition?

ebola
 
Well I was wondering what downstream effects amphetamine had that inhibits cannabinoids paycohlogical actions because in theory the opposite should potentiate the cannabinoid thus making it more effective I just think its more than monoamine release more likely its a downstream action of seratonin dopamine or norephinephrine
Really I think it has to do with amphetamine causing a ca+2 influx at nmda receptors because one of the main effects I get is a dissociative headspace and I believe it is achieved through Downstream cannabinoid activity on knew receptors
While seratonin release NE release and d1 agonization all cause an increase in glutamate but I will add this post is completely speculation and my opinion of this topic
 
Really I think it has to do with amphetamine causing a ca+2 influx at nmda receptors because one of the main effects I get is a dissociative headspace

Would you like to provide some evidence for this thread, or is it going to be entirely anecdotal?
 
If there's a question in here I didn't find it...
"What are the potential reasons (if any) that amphetamine reduce the effects of cannabinoids?"


^ That's the question OP is asking. I think this is a great thread - OP, maybe change it's title to the above sentence for easier reading? :)

I definitely notice a significant alteration of the effects of cannabinoids, while under the inflluence of amphetamine (and other 'vanilla' stimulants too - cocaine, pyrovalerones, etc).

I'm not sure I agree that it's simply because of "opposing forces" neutralizing each other, like with a benzo + amphetamine combo. I can still get high, from marijuana or synthetics, when on amphetamines - sometimes pretty high doses too (180mg+ 'mixed salts' sniffed throughout a couple hours). However, the cannabinoid experience is different in a way I wouldn't describe as simply "less strong". There is a concrete shift in the kind of high that is produced - the effects usually just kinda add some euphoria to the amphetamine push, especially when you're a little past the 'peak' of the amphetamine coaster. There is very little "day dreaming", and thoughts flow easily, but in a structured way; this is in contrast to how my thoughts flow when on a cannabinoid without amphetamine - giggly and lucid, yet the attention span of a baby goldfish. 8( =D

Still, in my head, I am sober (not in a technical way: even though I'm probably having a blast, my headspace is fairly straight and without the amphetamine I would probably feel "fucked up" or impaired)

One could argue that this is merely the amphetamine doing it's job: after all, I am prescribed adderall xr for ADD-NOS [alongside a SSRI and mood stabilizer for Bipolar-NOS, but I doubt that comes into play]. Still, I feel that this by itself cannot account for the entirety of the drastic change in subjective effects.

I rarely smile or joke around when stoned and on amphetamines, but just plain stoned I'm constantly fucking with people's heads and messing around :p
 
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