has to do with coupling to signalling pathways
hey,
this isn't really a complete theory, but i'd say it would serve as a crude explanation here.
take your dopamine receptor. when dopamine (DA) binds, a conformational (shape) change is induced in the cytoplasmic domain of the receptor which causes appropriate G-proteins to be attracted to the dopamine receptor (DAR) to get activated. For example, the G-protein "Gs" activates an enzyme (adenylate cyclase) which in turn produces the second messenger signalling molecule cAMP.
There are around 4 or 5 G proteins which are commonly used (and likely many more,) which all exert different effects. It is possible and likely that receptors may activate more than one G protein, and also miscelaneous "g-protein associated proteins," which will alter the activity of G-proteins.
The conformational change induced by the agonist on the receptor is a function of the structure of the agonist. What I am saying, is that a DA agonist, such as quinpirole, likely induces a different DAR conformation than DA will. This in turn will lead to the recruitment of a different set of signalling molecules to the receptor.
This means that a different response in the post synaptic cell may be elicted by various agonists.
More evidence of this kind of thing can be evidenced by differential tolerance mechanisms to different opiod agonists. Morphine does not cause receptor downregulation, where etorphine does. (It is proposed the morphine tolerance may be mediated by regulating levels of adenylate cyclase. this is similar to cannabinoid tolerance, actually.)
These differential tolerance mechanisms can be interpreted as the result of recruitment of signalling proteins by various mu opioid receptor - ligand complexes.
if anyone has any comments on that i'd love to hear them