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 GABA-A receptor (GABA-A-R) subtype. GABA-A-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 substance abuse. The GABA-A-R is a multimeric subunit complex. To date six alphas, four betas and four gammas, 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 beta-subunits results in the expression of functional GABA-A-Rs sensitive to GABA. However, coexpression of a gamma-subunit is required for benzodiazepine modulation. The various effects of the benzodiazepines in brain may also be mediated via different alpha- subunits of the receptor (McKernan et al., 2000, Mehta and Ticku, 1998, Ogris et al., 2004, Pöltl et al., 2003).
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 GABA-A receptor (GABA-A-R) subtype. GABA-A-Rs are
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