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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 substance abuse. The GABAA-R is a multimeric subunit complex. To date aix 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 GABAA-R 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). Lastly, phosphorylation of beta-subunits of the receptor has been shown to modulate GABAA-R function (Brandon et al., 2003).
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