Thats surprising considering how similar their effects are.
LSD has about 8 times the affinity for 5-HT2A as D3, vs 25 times for psilocin. This doesn't tell us anything about how they act on the receptors, or the affinities of the endogenous ligands they're competing with, but I think it's unlikely the dopaminergic activity is significant for either drug.
Edit: This does cite a paper from Nichols' lab which claims LSD has a second phase of action after the serotonergic phase, where its dopaminergic activity dominates. This strikes me as plausible... I'd have to read it.
Amphetamines, like all phenethylamines typically, are not direct-acting sympathomimetic, but indirect-acting; amphetamines elicit their effects through blockage and reversal of NET and DAT, the norepinephrine and dopamine transporter proteins. They are, however, TAAR1 agonists, which is currently thought to be partially responsible for regulating downstream effects on dopamine neurotransmission.
LSD is best described as a lysergamide.
Why does smoking have an immediate intensification effect when combined with lysergamides? Is it because of the combination of partial antagonism and down regulation blocking of certain receptors?