If D1 receptors stimulate adenylate cyclase (through GPCRs) and D2 receptors inhibit it, then why do mutations in both have similar effects?

Question

D1 and D2 both refer to specific types of dopamine receptors.I'm sure it has something to do with the fact that the D1 receptors are in regions different from D2 receptors.I know that adenylate cyclase usually triggers a signal transduction cascade that leads to increased cAMP+calmodulin, resulting in increased gene expression of proteins that help promote long-term potentiation of postsynaptic neurons (presumably lowering the absolute value of the voltage threshold that's needed to trigger another action potential, which increases neuron excitability).But an increase in dopamine is going to cause more neuron excitability in postsynaptic neurons in some regions (those that have D1 receptors), and less in others (those that have D2 receptors). What then explains the fact that increased expression at all dopamine receptors can help modulate attention span? I know that D3 and D4 are also involved, but they have to be either excitatory, inhibitory, or neutral.

Answer 1

Not only are the D1 and D2 receptors located in different regions, they are located on different parts of the neuron and control different aspects of neuronal function. D1-like receptors are mainly postsynaptic and are excitatory whereas D2-like receptors are both pre and postsynaptic and are inhibitory (inhibits cyclase).

This makes the answer to your question rather complex, so I'll leave it to you to decipher effects of mutations on these receptors.