GABAA Receptor 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 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 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-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) .

The antibody has been directly tested for reactivity in Western blots with rat tissue. It is anticipated that the antibody will react with bovine, canine, chicken, human, mouse, non-human primate, Xenopus, and zebra fish based on the fact that these species have 100% homology with the amino acid sequence used as antigen.

Brandon NJ, Jovanovic JN, Colledge M, Kittler JT, Brandon JM, Scott JD, Moss SJ (2003) A kinase anchoring protein 79/150 facilitates the phosphorylation of GABAA receptors by cAMP-dependent protein kinase via selective interaction with receptor β -subunits. Mol Cell Neurosci 22:87-97.

McKernan RM, et al. (2000) Sedative but not anxiolytic properties of benzodiazepines are mediated by the GABAA receptor α1-subtype. Nature Neurosci 3:587-592.

Mehta AK, Ticku MK (1998) Prevalence of the GABAA receptor assemblies containing &#9451-subunit in the rat cerebellum and cerebral cortex as determined by immunoprecipitation: Lack of modulation by chronic ethanol administration. Mol Brain Res 67:194-199.