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Does 2CB work on serotonin?

Honestly I'd think there has to be some sort of stimulant effects to some of the 2c-'s. Physically it feels like a stimulant to me, can those effects come purely from 5-ht2 receptor activity?
 
lolusername said:
Honestly I'd think there has to be some sort of stimulant effects to some of the 2c-'s. Physically it feels like a stimulant to me, can those effects come purely from 5-ht2 receptor activity?
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When it's said that 2C-B has serotonin receptor affinity, that does not mean it is the only thing it does. Pretty much all psychedelics have some sort of secondary effect because they also bind slightly to other receptors.
Some like LSD are very promiscuous meaning that it binds to a lot of different types of receptors yet the most remarkable and primary psychedelics effects are thought to be caused by the activation of a specific kind of serotonin receptor: namely 5-HT[2A].
Others like the NBOMe compounds are quite selective instead of promiscuous meaning that the binding to 5-HT[2A] is relatively strong compared to other things it does. But even those compounds have "hidden agenda's". Of course I don't mean that they have conscious intentions but that there are actions on receptors that were not particularly wanted by users of the compound. Or even worse: those secondary effects can be the cause of side-effects that can range from unpleasant to deadly.

So to sum up: 2C-B does other things as well besides acting on the receptor that is associated with psychedelic effects.

And another thing: there is a cascade of effect. When a psychedelic (like 2C-B) acts on 5-HT2A, there is often a domino effect of activation spreading to other neurons that are necessarily serotonergic. This is not random, it's not like any kind of receptor can be affected by secondary domino-like spreading. You should consider activation of 5-HT2A (serotonergic) as a part of a stimulating system. If I'm not mistaken this is more or less meant by the sympathetic nervous system. I don't want to oversimplify but this system has a stimulating nature, it is countered / complemented by the parasympathetic nervous system with is the opposite of stimulating. Naturally these systems are in balance but all kinds of causes can make the balance lean more to stimulation or more to sedation.
Causes can be "external" like being witness to a violent crime or being in a horrible accident. Such a thing will trigger the balance in all kinds of complex ways to lean strongly to the stimulating side to make you more adequate for proper reaction to what is happening. Doing soothing things are the opposite and elicit the balance of the sympathetic and parasympathetic nervous system to lean more to the sedating side.
These things are pretty complex, for instance both systems can have unpleasant sides as well as pleasant sides which are reflected in several ways:
For instance think of being in an accident like I mentioned, this will trigger stimulation in a way that is harsh and for instance boosts your adrenaline and noradrenaline without boosting the release of neurotransmitters that take the edge off. Nature adequately programmed us to be alert only.
Now think of exercizing. You also feel stimulated but in a more balanced and less harsh way, because there is no particular alarm involved. If your muscles start to burn this is eventually soothed by what is called the "runner's high" which I think is caused by the release of natural painkillers (endorphins which are a bit like your body's own opiates).
To sum up: there is a whole spectrum of sensations and also combinations of those sensations depending on the particular situation. And this spectrum can be 'mimicked' by taking drugs that affect the same receptors that are involved with naturally occuring events. You can simulate a "runner's high" or only a part of it, and you can imagine countless other sensations which may or may not be paradoxical in some way.

The cascade (domino) effect is a weak argument though because not every 5-HT2A agonist produces a proportionally equal cascade effect. I'm not sure if this can be explained by the exact affinity having different kinds of cascade effects but I think it's not a huge contributor to the way psychedelics differ in side-effect. But it is still a real part of the picture.

To return to the original point: 2C-B does not only act on 5-HT2A and I don't think there is any known compound which is absolutely 100% selective for that receptor.
I'm gonna go out on a limb here and say: It seems though that the more selective a compound is for it, the more it feels like a pure and clear psychedelic. NBOMe's are described that way, but they are tricky: there seems to be a small margin that can make the side-effects too heavy. Also it doesn't explain why the promiscuous LSD feels so pure and clear but I think it must have something to do with the extremely low doses at which they act. But enter mescaline, which has a very high active dose yet it feels very pure and clear. I think the explanation for that is that it has a favorable profile and most secondary actions have a neatly empathogenic effect instead of speedy and potentially panicky or stim-psychosis like (think of DOI, DOB and DOB-dragonfly mostly but not limited to those).

So, lolusername, in answer to your remark that 2C-B feels quite like a stimulant: I guess it is some kind of combination of the mentioned domino effect but mostly the fact that it activates other sympathetic CNS receptors. But it apparently does so in a favorable way considering the fact that 2C-B is well tolerated by most people so I think it must target other 5-HT receptors than the 2A subtype but not things like NE receptors to a significant extent.
 
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