In heterologous expression systems, EtOH has been shown to inhibit responses to activation of GPCRs that couple to Gq-like G proteins. These findings mostly involve demonstrations that pharmacologically relevant concentrations of EtOH reduce the ability of the GPCRs to activate a calcium-dependent chloride current in the Xenopus laevis oocyte preparation (Minami et al. 1997a, b, 1998). Among the GPCRs that have been examined in this context are metabotropic glutamate receptors (mGluRs), muscarinic ACh receptors and serotonin type 2 receptors. The observation that these three receptor effects are all inhibited despite differences in the structures of the receptor molecules themselves, indicates that the EtOH target site is likely downstream of the receptor itself. Indeed there is some evidence for involvement of protein kinase C, at least in the inhibition of muscarinic AChR-induced responses (Minami et al. 1997b).
