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Why do different dissociatives have such different effects?

Artificial Emotion

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The three common dissociative drugs, PCP, N2O and DXM all antagonize the NMDA receptors in the brain to varying degrees apparently, but each have completely different subjective effects/highs. Why is this? Why do they appear to have vastly different effects? Please forgive my ignorance. I know very little about this subject area.
 
I'd say ketamine was more common than PCP by a long way. Interesting question though. I suspect that the serotonergic (and undoubtedly other chemical) effects of PCP and DXM make a huge difference to the effects but have little real knowledge of the way they work myself.
 
I ALWAYS wonder these similar kinds of things...

for example, how do psychadelic drugs induce unique visuals between themselves, even though they agonize the same receptors? :P
 
The effects of nitrous are a lot more complicated as well. At the very least it activates potassium channels, the chances are there is a lot more going on besides.
 
I ALWAYS wonder these similar kinds of things...

for example, how do psychadelic drugs induce unique visuals between themselves, even though they agonize the same receptors? :P

it probably comes down to how full the agonism is, and the specific combination of receptors and receptor subtypes that are affected.

And in the end, even the same exact drug taken twice in the same dosage and setting can have drastically different effects.

I think this may be one of those things that are far too complex to ever fully have a scientific grasp of all the workings. (not to say science shouldn't keep working towards that grasp)
 
I'd say ketamine was more common than PCP by a long way. Interesting question though. I suspect that the serotonergic (and undoubtedly other chemical) effects of PCP and DXM make a huge difference to the effects but have little real knowledge of the way they work myself.

Sorry I meant to include that actually.
 
The same question could be asked of all psychotropic drugs, in that there are families of drugs which target specific brain regions and receptors, and yet have different effects.

There are a number of complexities to take into consideration such as those highlighted above, and once equated for, you can begin to investigate the connundrum you pose . However, in terms of the comparison of the effects of drugs that affect the same receptor, there is one answer that is plainly obvious to me: if you are dealing with a different drug, you are dealing with a different molecule, and differing molecules have differing properties of interaction with other molecules at the atomic level - in this case, complex molecular structures which we call proteins that make up the binding ports for nerve receptors.

Specifically, if we keep one thing constant - the receptor (sub)type - and vary the drug molecule for the same target receptor, we can see that the variables have different 'affinities' for the constant. The variables also can be seen to have changed kinetics and dynamics for the constant; in vitro pharmacological studies over the decades show us the vast differences between these properties of 'similar' drugs.

The dynamics and kinetics of molecular biology is a whole area of study in itself, and is far too deep to go into in a post, however, I highly recommend that anybody interested in the reasons why different drugs - which at a superficial glance appear to have similar physical properties - actually behold a vast spectrum of activities at the atomic level, research this area thoroughly.
 
As others have said, drugs mostly effect more than just one receptor type, and do so in different ratios. Particularly with dissasociatives - we just lump anything that acts primarally on that receptor into the classification of "dissassociatives", when in fact they are very different chemicals, which probably get distributed completely differently within the body.

The real wonder is not that they all produce such different effects, but that such completely different chemicals all effect the same receptor at all!

What i really wonder about is psychedelics - we have all these phenethylamines, (and all these tryptamines). Chemically _VERY_ similar, all act on the same receptor. All have very similar effects, but there are undeniable differences between them. We can explain (without certainty of accuracy) that some are more "speedy" because they have dopaminergic effects... but what makes one phenethylamine more visual than another? Why do some tryptamines produce auditory effects?

There's a real lack of understanding of brain chemistry, despite huge amounts of research done for antidepressant and anti-psychotic medications (both of which are hugely profitable). I'm sure if psychedelics were legal, they'd be every bit as well researched (there's certainly money in it), and we'd have answers for these questions, and mankind would be better off for it.
 
True, D9. But I don't really know the reason for that either with any level of real understanding so these question interest me too. Nice to read condensed versions of such complex things that are a lil easier for the layman to get their heads around than chemistry textbooks :D
 
Yeah true, sorry.
It's probably a complicated thing. Off the top of my head I would guess it has to do with the different receptors they affect and differences in binding affinities, polarity, chirality, solubility, half-life, the way it's metabolized, etc. Stuff like that.
 
I don't find the effects to be "completely different". Different yes, but ketamine, nitrous and dxm all remind me quite a bit of each other.
 
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