Carbamazepine and electroconvulsive shock attenuate beta-adrenoceptor and muscarinic cholinoceptor coupling to G proteins in rat cortex.

We have recently found that lithium attenuates the function of G proteins, suggesting these proteins as the common site for both the antimanic and antidepressant therapeutic effects of lithium. Perturbation of G protein function may thus be a general characteristic of treatments effective in bipolar affective disorder. In the present study, we demonstrate that both chronic carbamazepine and repeated electroconvulsive shock treatment inhibit the coupling of both muscarinic cholinoceptors and beta-adrenoceptors to pertussis toxin-sensitive and cholera toxin-sensitive G proteins, respectively.