Anti-GABAA Receptor δ, N-Terminus Antibody

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 αs, four βs and four γs, 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 α- and β-subunits results in the expression of functional GABA-A-Rs sensitive to GABA. However, co-expression of a γ-subunit is required for benzodiazepine modulation. The various effects of the benzodiazepines in brain may also be mediated via different a-subunits of the receptor (McKernan et al., 2000; Mehta and Ticku, 1998; Ogris et al., 2004; Pöltl et al., 2003). More recently there have been a number of studies demonstrating that the δ-subunit of the receptor may affect subunit assembly (Korpi et al., 2002) and may also confer differential sensitivity to neurosteroids and to ethanol (Wallner et al., 2003; Wohlfarth et al., 2002).