Kaleida
Bluelight Crew
- Joined
- Sep 6, 2015
- Messages
- 2,806
Interesting, so how does the full agonism of a research paper differ from the ordinary view, and if they are not more powerful at activating the 2A, then why are they used in research papers as full agonists? And what causes the toxicity?
It mostly just boils down to the fact that the way they're using the term "full agonism" in this context has to do with the drug's capacity to activate the brain preparations fully in a way comparable to serotonin when paying attention to second messenger levels like inositol phosphate. The difference is just that when they're testing drugs this way, they can easily send it right to the relevant site and don't worry about things like overdosing or anything and in general, like I pointed out with the data on LSD, psilocin, and mescaline, pretty much any 5-HT2A receptor agonist can get to or near "full agonism" when you can test them that directly and without any restrictions. It's useful for testing things like how the 5-HT2A receptor functions in various parts of the brain without having to worry about how the living animal responds to the drug and just being able to test the exact part of the brain or specific cell type of whatever that you want to test. Again, I'm no professional and I'm sure they could come up with many more ideas off the top of their head of things you can do with this kind of info, but basically it's just for brain research, and the way they're using it in that kind of research, it does function as a full agonist when administered at a high enough concentration, so it counts.
When it comes to drug users, the definition of "full agonist" is usually used more so with respect to how much the drug actually activates the receptor inherently instead, at least based on the conversations I'm familiar with. It's an important question when it comes to varying levels of safety with things like morphine vs mitragynine (from kratom) or THC vs synthetic cannabinoids. These are the kinds of differences in the psychedelic molecules that the study I linked before supposedly measures specifically. This all basically just suggests that NBOMes are not "full agonists" in the way that a lot of people outside of the scientific community originally interpreted them to be, but really, that doesn't change a whole lot about what we know about them anyway, because a lot of what people assume to be true about "5-HT2A receptor full agonists" was really just coming from NBOMes in the first place. The truth is, at least to my knowledge, there's yet to be much scientific consensus on the difference between 5-HT2A receptor full and partial agonists, probably especially because psychedelics are highly complex drugs that can also work through multiple channels at the same receptor, like it's possible to be a full agonist at one signalling pathway at the 5-HT2A receptor and a partial agonist or even antagonist at another.
The reason that NBOMes are used in scientific research is for their 5-HT2 receptor selectivity. The more receptor targets or other site a drug binds to than the specific one you're interested in, the less you can trust that the data from your research actually does have specific relevance to the receptor you're interested in compared to the other targets, making selective tools like the NBOMes significantly better for testing 5-HT2 receptor activity than almost any other psychedelics. The toxicity of NBOMes is not considered to be understood by any scientific body that I'm aware of. I wouldn't be surprised if it is through 5-HT2 receptors, but the explanation for how exactly it works would still not be entirely clear yet given that, as again psychedelics can do rather complex things at those receptors involving different affinities and efficacies for different pathways there simultaneously.
Salvia killed people too. Doesn’t matter that they (just) should have had a trip sister, it’s just same as saying (and I do claim so and am sure about it) that no one would have died from nbome’s if they were available only in microgram range doses prepared for nasal use and kept for very experienced people only.
You’re welcome to think those two situations are comparable if you like, but I personally do not.
Which are safe dissos and which not? Care to recommend?
Would be great to know which RC disso wont cause a lot, possibly reversible damage if used regularly or in high doses. Make some RC as popular as nbome’s, leave it on market for long enough and there's good chance it’ll turn out just as terrible as nbome, that’s the nature of the game, long gone are days of “research chemicals” that were really researched before becoming widespread, like 2c-b, αMT or 5-meo-dmt.... Sure you can convince yourself shit like if αMT was good and safe, 5-meo or 5-cloro must be too, you wish.. There’s some basic logic about what’s probably safe what’s probably not safe but before real research it’s just guessing and at level of users, usually just self delusion.
I don't use research chemical dissociatives because I have the exact same mindset about them that you do.
I also remember friend begging me to get 2c-x so he could make “new acid”, and it turned out it wasn’t “new acid” nor “better than mescaline”, in fact it was mostly just a “new cheap drug” almost always sold at best dosed at least 2 – 3x times too strong (part of reason for that is that blotters aren’t really perfect delivery form for sublingual use of drug) and at worst just as acid.
I didn’t really care too much for nbome’s but 300mics of 25c made for a great night, euphoric and with lot of music appreciation and few times mix of different nbome’s in mg range made for interesting but experience with a lot of body load, waaaaaaaaaaay more then bromodragonfly produces.
I never actually tried NBOMes myself so I have no direct opinion on them. I’m glad you got something out of them even if they weren’t the very best.