Interesting thread with back and forth banter: http://www.bluelight.ru/vb/archive/index.php/t-494408.html
Research leads me to conclude that:
D2 is at the very least an additional hallucinogenic receptor, if not the only hallucinogenic receptor. It causes dissociative hallucinogenic states (blocks NMDA's effect, causes visuals through an unknown mechanism). 5-HT2A increases the production of anandamide through its signal cascade, which, when combined with other signals, would lead to increased activation of D2 receptors. Since 5-HT2A agonists also enhance your intelligence, I figured the mechanism for that would be enhanced glutamate activity. I think it's in one of those articles I posted, but either way I found evidence that 5-HT2A actually does enhance the activity of both AMPA and NMDA receptors.
Kappa Opioid Receptor's main function is to shut down dopamine neurons by releasing GABA, and to upregulate D2. The shutting down of dopamine neurons causes the characteristic dysphoria of dynorphin, Salvinorin A, DXM, etc.
D1's main function is to cause euphoria, but when activated it also signals NMDA receptors to activate, which decrease the dopamine receptors on the cell (does it also increase AMPA, or are there no AMPAs on dopamine cells?)
D2's main function is to block the NMDA signal on the dopamine neurons so the "habit" can go away (downregulating AMPA? or are there only Dopamine receptors on dopamine neurons?), but it also causes visuals. It also upregulates D1 receptors (restoring the normal sensitivity of dopamine neurons?).
No idea about D3 and 4 yet. haha
Mu Opioid receptor releases dopamine and inhibits GABA release in dopamine neurons, which leads to increased addictiveness (more NMDA signaling in dopamine neurons means increased signal strength (habit), but also means decreased number of dopamine receptors (tolerance)).
CB1 and CB2 are analogous to Mu opioid and Kappa Opioid receptors but without bad effects (for the most part; I may be wrong lol). One would release phenethylamine while the other would upregulate D2 receptors. D2 stimulation would produce visuals and dissociation (the dissociation would be from NMDA effect blockage, which would fix D1 receptor levels and AMPA levels). Phenethylamine also causes euphoria by increasing the outflow of dopamine into the synapse.
According to this: http://www.ncbi.nlm.nih.gov/pubmed/18160635 Dopamine neurons do have AMPAs as well as NMDA, glutamate, and dopamine receptors, so that part of my theory still stands.
This means THC works by upregulating D2 and releasing Phenethylamine. Phenethylamine releases dopamine which binds to D1 and other receptors. D1 on its own would cause D1 to downregulate. But PEA also binds to D2, which causes visuals and dissociation (potentiated by the other effect of THC). The dissociation, from intercepting the NMDA signal (not directly blocking it, but affecting the signal downstream), causes the dopamine receptors to reset (but also downregulates D2, haha).
Salvia would work through a similar mechanism, (KOR upregulates D2, D2 causes visuals and dissociation) but while causing dysphoria instead of euphoria (caused by KOR releasing GABA into Dopamine neurons). Its mechanism greatly increases the visuals over THC, though, which is a plus.
LSD is known to have a two-stage effect: first of 5-HT2A receptor stimulation, and second of D2 receptor stimulation. I'm guessing this has to do with a metabolite (which might explain why it lasts for so long compared to other molecules? not so sure about that though). The effects are mental and stimulating at first, then relaxing and (according to theory, but haven't verified this part yet) dissociating. Some reports indicate that mental stimulants (activating the glutamate system like the initial 5-HT2A phase does) destroy the relaxing spiritual phase of LSD, which would mean they block the dissociating NMDA inhibition. This gives evidence for and against the theory of D2 being the core hallucinogenic receptor, with 5-HT2A activating it. It's a nice theory, but I just want the truth.
Mescaline binds to both 5-HT2A and to D2. It would have both effects from both receptors.
Tryptamines bind only to 5-HT2A, but they also bind to D1 (which doesn't cause hallucinogenic effects, but euphoria! hahaha).
So the theory is that D2 causes the enhanced spiritual effects (visuals, ineffable experiences, seeing God, enhanced perception of music, etc.) and dissociation by blocking NMDA's effect, and 5-HT2A merely activates D2 while enhancing it through engaging the glutamate system to enhance intelligence. Hopefully we can verify or disprove this theory.
This all shows that Ketamine/ Methoxetamine are the perfect anti-addiction aids. They activate KORs to upregulate D2, activate Mu Opioid to prevent the dysphoria from KOR and to add in some euphoria from dopamine release, activate D2 to upregulate D1 (also causing fun visuals) which blocks NMDA's upregulation of AMPA (causing the "habit" to go away). They enhance this effect through directly antagonizing NMDA as well. All of these effects combine to completely reverse addiction while blocking tolerance and withdrawal symptoms at the same time, and providing euphoria and psychedelia as well. This is better than a pure NMDA antagonist (which helps, but not as much). Methoxetamine is less toxic (and more legal) than ketamine, which makes it PERFECT for anti-addiction (both to prevent it before it happens and to reverse it after it happens). It might not be as 100% effective as ibogaine, but it's certainly a LOT more enjoyable and a lot more repeatable.
This also explains a lot of the effects of schizophrenia. It could easily be caused by upregulated dynorphin from excess stress, which would constantly upregulate and activate the D2 hallucinogenic receptor while keeping the dopaminergic neurons suppressed causing dysphoria. This doesn't explain everything, as there is likely an anticholinergic effect at play, but it does play its part.