Anti-GABA (A) alpha1 (ext.)

IC, IF, IFC, IHC, LCI, WB

γ-Aminobutyric acid receptor type A subunit α1, GABRA1

Shipped at room temperature. Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C

Lyophilized powder. Reconstituted antibody contains phosphate buffered saline (PBS), pH 7.4

γ-Aminobutyric acid receptor type A subunit α1, GABRA1 - A Rabbit Polyclonal Antibody to GABA(A) α1 Receptor

Mouse - identical; human, bovine - 16/17 amino acid residues identical; chicken - 14/17 amino acid residues identical

Confirmed by amino acid analysis and mass spectrometry

0.8 mg/ml

Extracellular, N-terminus

Rat

41116161

GABA (γ-aminobutyric acid) is the major inhibitory neurotransmitter in the brain. Its production, release, reuptake, and metabolism all occur in the nervous system.1The GABA transmitter interacts with two major types of receptors: ionotropic GABAA receptors (GABAAR) and metabotropic receptors (GABABR). GABAARs belong to the ligand-gated ion channel superfamily.2 GABA inhibits the activity of signal-receiving neurons by interacting with the GABAA receptor on these cells.3 Binding of GABA to its GABAA receptor results in conformational changes that open a Cl- channel, producing an increase in membrane conductance that results in inhibition of neural activity.2GABAARs are heteropentamers, in which all five subunits contribute to pore formation. To date, eight subunit isoforms have been cloned:α, β, γ, δ, ε, π, θ, and ρ.1 Six α subunit isoforms have been found to exist in mammals (α1-α6). In most cases, native GABAA receptors consists of 2α, 2β, and 1δ subunits. The α subunit is the most common and is expressed ubiquitously. It determines the affinities of GABAARs for allosteric ligands.Each subtype has a unique regional expression in the brain, and individual neurons often express multiple subtypes.4 The α1 subunit is highly expressed in adulthood while the α2 subunit is highly expressed very early in rat brain development. Failure to complete the normal transition between the α-subunits that are highly expressed in early development (α2, α3, and α5) and those expressed in adulthood (α1) is suggested to play a major role in the development of temporal lobe epilepsy.5