>>14270107>there is no clear correlation at all between all 5ht2a receptor agonism, antagonism, inhibition, modulation and the psychedelic experienceThat's just blatantly incorrect. There is a lot of evidence that 5HT2AR agonism plays a major role. For one, binding affinities on this receptor and potency correlate well. Next, you can reduce head-twitch - the classic indicator for psychedelics - by knocking out SERT in mice (which reduces 5HT2AR density). Next you can give selective 5-HT2AR antagonist like volinanserin to a subject on LSD, and the effects stop. Next, you can give a selective 5-HT2CR antagonist and the effect do not stop. Next, the highest activity is observes in brain regions that have the highest density of 5HT2AR, such as the prefrontal cortex and the neocortex.
>THC even stimulates them it and yet you likely know its its more sedative than psychedelic at high doesesAnon, THC primarily acts on CB receptors. You could just as well say that PCP or salvinorin A or scopolamine don't behave like classical psychedelics either, but is that surprising when they mostly act on NMDAR, kappa-opioid-receptors or the cholinergic neurotransmission respectively? THC doesn't seem to have high affinity for that receptor, it could interact indirectly (via allosteric modulation for example) or other effects, but it's at best a modulation mediated mostly by CB agonism.
>>14270212This is true.
