Although the β1 subunit is less abundant than the other β subunits, it is likely that some β1-containing GABAA receptors exist, based on regional distribution and coimmunoprecipitation data (Li and DeBlas, 1997; Jechlinger et al., 1998). A potential pharmacological fingerprint, salicylidene salicylhydrazide, has been reported to be a negative allosteric modulator selective for β1 versus β2 or β3 subunit-containing receptors (Thompson et al., 2004). There is some evidence (Whiting et al., 2000) that cultured astrocytes express GABAA-R with α2β1γ1 combination, and they are uniquely enhanced by the benzodiazepine site ligand DMCM, a β-carboline. However, more evidence is needed to establish if this subtype actually exists in the brain. We therefore placed just one subtype for αβ1γ/ αβ1δ in category B.
