**This antibody is a replacement for our original catalog #868-GDN. It was produced by the same methods, using the same fusion protein antigen in new animals. The application dilutions are from #868-GDN.Pooled Serum
- Affinity Purified from Pooled Serum
- Species Tested:
- Mouse, Rat
- WB 1:1000IHC 1:200**ICC 1:500** Don't see your application?
- Host Species:
- Rabbit Polyclonal
- Gene Name:
- Molecular Weight:
- ~50 kDa
- Cite This Antibody:
- PhosphoSolutions Cat# 868A-GDN, RRID:AB_2631037
The antigen is a fusion protein from the N-terminal region of the δ-subunit of rat GABAA receptor.
The antibody is prepared from pooled rabbit serum by affinity purification using a column to which the fusion protein immunogen was coupled.
Biological Significance: ExpandCollapse
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 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 GABAA-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).
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