I guess "HT[subtype number][sub-subtype letter]" works, since 5ht is short for "five hydroxyl tryptamine", and the 5ht is prominent enough to claim to be "the" hydroxylated tryptamine. It's potentially confusing, though, as histamine receptors are abbreviated with "H[number]".
D2 could in fact be the psychotomimetic receptor but Bromocriptine, being what it is, doesn't hit it for the sole reason of it being a mellow, sedating drug, not a psychotomimetic drug.
We have to take care to avoid using subjective effects to characterize physiological activity, as history is littered with examples of mistaken but long-held confidence in erroneous explanations drugs' mechanisms (eg people tend to circulate misinformation that 2cb releases monoamines because it feels a bit entactogenic). Bromocriptine is actually a strong agonist at D2 (PDSD database). In fact, this is B's strongest activity aside from binding at a couple adrenal receptor subtypes (ibid).
Now, I think "psychotomimeticism" is too vaguely and nebulously defined to lend itself to categorizing compounds (and also too unreliably induced by said compounds). Imagine, for example, 3 people experiencing a "psychotic break", one on PCP, one on LSD, and one subject to forced sleep-deprivation. The symptoms between the three will prove quite distinct, particularly the types of hallucinations encountered. The only reliable similarity between the three is that there is
some break from consensus sensory experience and beliefs about the world, centering (mostly) on the person experiencing psychosis (eg, schizophrenics tend to consider themselves uniquely subject to disproportionate surveillance due to personal characteristics or actions that make them unique).
Because of the conceptual and empirical challenges presented by analysis of psychosis, I don't think that there could be a single receptor sub-type that mediates the affliction. I think that we'll discover the underlying cause of schizophrenia (rather, the most directly relevant mechanism) when we reach moderate proficiency in understanding patterns of activity in neural circuits as a meaningful, systematically theorized domain with empirical linkages to subjective experience .
You could have something with the exact same binding affinity to BC that acts in a completely different way.
This is likely what's going on with lisuride. A compound with a given affinity can be an agonist, partial agonist, antagonist, or inverse agonist. But beyond this, some agonists initiate secondary-messaging cascades distinct from the endogenous ligand, as is the case with classical psychedelics (with selectivity for PLA2-mediated increase in arachadonic acid activity over PLC-mediated PKC activity). Lisuride, IIRC, is selective for PLC-activition (5ht itself activates both, probably with some selectivity for PLC-mediated cascades).
For instance, I was thinking earlier that if a different synthesis route to LSD that brings up 100% LSD could have slightly different effects to another route of 100% LSD, like if you bake a cake with more water than another; it is less dry than another. It's a basic analogy but the theory behind it could go a lot deeper.
Chemical synthesis tends not to be analogous to culinary preparation in this way. Alter the 'ingredients' that go in or their amounts, and you get additional unreacted intermediaries, novel chemical reactions that lead to additional intermediate compounds, prevention of reaction from precursor to product (at whatever stage, involving whichever intermediaries), no change in the reaction, etc. The goal of synthesis production of a single, isolated compound, and this compound cannot change unless one reacts it to or replaces it with an entirely different compound; eg, I cannot make a "slightly different" r-DOB but only other compounds entirely. If I go around tweaking with the brominated reagent involved, let's say replacing it with an iodine-bearing reagent, I can prevent the reaction from occurring or yield an alternate product (eg,DOI), but I can't make a 'different' DOB.
It's only when you just happen to have unreacted precursors or intermediate compounds that are psychoactive at low doses
combined with negligence in performing the final solvent washes that different 'cooks' take on discernibly different 'flavors'. Eg, meth containing 50 percent unreacted pseudoephedrine will feel different. However, because such phenomena are by nature difficult to control, synthetic chemists avoid allowing impurities to persist in their products. Doing so increases the desirability of their product, and thus their profit.
Also I'm no scientist either, just an avid user!
Me as well (my training's in sociology)! Please never let that discourage you from asking questions here.
ebola
Okay so that study is not very credible?
