Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system, causing a hyperpolarization of the membrane through the opening of a Cl- channel associated with the GABAA receptor (GABAA-R) subtype. GABAA-Rs are important therapeutic targets for a range of sedative, anxiolytic, and hypnotic agents and are implicated in several diseases including epilepsy, anxiety, depression, and sub-stance abuse. The GABAA-R is a multimeric subunit complex. To date six (s, four (s and four (s, plus alternative splicing variants of some of these subunits, have been identified (Olsen and Tobin, 1990, Whiting et al., 1999, Ogris et al., 2004). Injection in oocytes or mammalian cell lines of cRNA coding for alpha and betasubunits results in the expression of functional GABAA-Rs sensitive to GABA. However, coexpression of a (-subunit is required for benzodiazepine modulation. The various effects of the benzodiazepines in brain may also be mediated via different (-subunits of the receptor (McKernan et al., 2000, Mehta and Ticku, 1998, Ogris et al., 2004, Pöltl et al., 2003). Anti-GABAA-Receptor, a1-Subunit Western blot of mouse forebrain lysates from wild type (Control) and a1-knockout ((1-K/O) animals showing specific immunolabeling of the ~51k a1-subunit of the GABAA-R. The labeling was absent from a lysate prepared from a1-knockout animals.