In the basal ganglia the effects of gamma-aminobutyrate (GABA) are mediated by both ionotropic (GABA(A)) and metabotropic (GABA(B)) receptors. Although the existence and widespread distribution in the CNS of the GABA(B) receptor had been established in the 1980s the field of GABA(B) research was revolutionized with the discovery that two related G-protein-coupled receptors (GPCRs) needed to dimerize to form the functional GABA(B) receptor at the cell surface. This finding lead to a number of studies of oligomerization in GPCRs and detailed pharmacological studies of the cloned receptors and their splice variants. Particular interest has focused on the proteins interacting with the receptor which may be important in mediating the longer term signalling effects of the receptor and modifying its cellular localization or physiology. The cloning of the GABA(B) receptors also lead to the identification of the first compounds interacting in an allosteric fashion with the receptor some of which may have therapeutic value. Most recently "knockouts" of both the GABA(B) subunits have been produced where in general as expected there is a loss of the majority of the inhibitory effects of the GABA(B) receptor.