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I've never been paranoid about synthetics because every time I bought (except once over the darkweb) I knew the dealer and he was a respectable man. I don't nessecarily have a problem with synthetic noids inherently, and in fact there are quite a few that I have interest in trying (such as JWH-018, HU-210) if I can ever buy just the lab made powder. But as the fruits of the different generations get outlawed, each successive generation gets worse and worse. The current generation is straight up horrifying, makes 25I and the rest of the NBOMes look safe. I'm talking about high risk of a lethal cardiac event, stroke, psychotic break. I wouldn't touch any synth noid past gen 3 even in a lab-pure powdered form. And in most instances, we aren't even talking about that. We're talking unknown amounts impossible to dose sprayed in combination with others on random plantmatter. I wouldn't even consider any synth noid UNLESS it was lab-pure powder that I had run through GC/MS for purity/identification reasons.
Also, I know salvia is commonly cited as a dissociative, but I would say its dissociative properties are the weakest. Its initial hallucinations are nothing like NMDA antagonists, they have far more in common with psychedelics. I would classify it as a deliriant first, especially because deliriants are the least typical of the 3 hallucinogen types, so its oddball set of effects fit just fine in the class that houses both GABA-rho agonists and anticholinergics.
Kinda. It's like when you run a really high fever that your worldview and logical process experiences a shift in perspective. If you try really hard you can stay grounded. I was somewhat aware I was experiencing a schizophrenia-tier delusion of persecution, but you can only be reactive to these kinds of events. Proactivity is only viable by not taking the substance. If you're weakminded it would be extremely easy to succumb to the delirium to an extent that will reap nasty consequences (like calling an ambulance because you thought you smoked a substance with high potential for lethality).
This experience was actually very important for me. I've fucked around with really nasty things like 25I and because they never really gave me troubles other than temporary anxiety attacks that I found easy to deal with even in the moment. I've always known the risks that are present with substance use and that this is a pretty dangerous game, but it never really clicked with me emotionally until that experience. Like, "Oh shit, things could have actually gone really fucking bad and fucked up my life for a while... if not just cutting it off right there. I should slow my roll a bit, until my circumstances change and I can minimize the consequences of these risks."
Not really. They just bind to those pathways and activate them. The different receptor types do different things in different parts of the brain (this is why we don't use dopamine agonists to treat ADHD) and often this is where the difference in effects of molecules come into play because they have natural gravitations in the CNS where they'll bind to their target receptors. The activation of these receptors is what causes the effects.
Delirium is thought to be caused by an imbalance between dompamine and acetylcholine systems. Kappa opiod receptors (salvia's primary target) have a lot of downstream effects on both of these systems. I know for a fact (though the specifics slip my mind) that it has pretty big initial effects with dopamine, specifically downregulation. I am unsure of the KOR's downstream effects on mACH, but if I'm remembering a paper I read recently, morphine is noted as having a stronger antagonistic affect on muscarinic receptors downstream than derivatives and if you'll allow me the liberty to do so, I hypothesize this is due to it's greater agonist affinity for KOR.
This is comparable to anticholinergics like scopolamine, diphenhydramine, etc. who cause delirium specifically by straight up blocking acetylcholinesterase (enzyme responsible for destroying acetylcholine, which is the neurotransmitter associated with ACH receptors).
Although, related to your analogy, I recall reading a paper somewhere that posited endogenous DMT's mechanism is as a cocktail of neurotransmitters used in the higher functioning parts of the CNS associated with sensory perception. In its normal, natural levels, it's likely a regulator of 5-HT. The actual paper went into details that unfortunately slip my mind, including voltage regulation and even went into such a depth that it posited explanations for why it is very promiscuous with the sigma 1 receptor. It was way over my head as a layman drug user, and I wish I could find it because it was super interesting and seemed very well researched and presented, but I just looked for like 40 minutes and couldn't find it. DMT is the only endogenous psychedelic (at least, commonly considered to be a psychedelic) and it's a very very unique one. Anyone who has taken it can attest that the hallucinatory state it produces is very different from virtually every other psychedelic, despite having pretty standard 5-HT agonism for the class.