mediated primarily by GABAA-Rs composed of α2 βγ2 subunits (Low et al., 2000), and, under conditions of high receptor occupancy, also by α3 GABAA-Rs (Dias et al., 2005; Yee et al., 2005). The α2βγ2 receptors are also implicated in some of the muscle relaxant activities of diazepam (Low et al., 2000). Receptors containing the α3 subunit seem to mediate the anti-absence effects of clonazepam, as indicated by the respective point mutated mouse (Sohal et al., 2003) and the α3 global knockout mice displayed a hyperdopaminergic phenotype relevant for GABAergic control of psychotic-like symptoms (Yee et al., 2005). The α5βγ2 receptors seem to influence learning and memory, shown by improved spatial memory in mice with knockout of α5 subunits (Collinson et al., 2002), and improved trace fear conditioning in the point-mutated α5 knockin mouse (Crestani et al., 2002). These and other studies for the first time indicated a possible function of specific GABAA-R subtypes in the brain and provided additional evidence for their actual existence in vivo.
