GABA(A) α1 Receptor Basic Research Pack

All You Need for GABA(A) α1 Receptor Research
  • Lyophilized Powder
  • Antigen Incl.
  • Bioassay Tested
  • Shipped at Room Temp.
Cat #: ESB-800
Sizes: 4 Vials
Last update: 04/09/2018

Alomone Labs is pleased to offer the GABA(A) α1 Receptor Basic Research Pack (#ESB-800). The Research Pack contains all you need for GABA(A) receptor research: GABA(A) α1 receptor-specific antibody and pharmacological tools all in one economical package!

For research purposes only, not for human use
Product NameCat #Size
Anti-GABA(A) α1 Receptor (extracellular) Antibody
AGA-001 1 x 0.2 ml
B-135 1 x 250 mg
G-120 1 x 10 mg
Scientific Background
Scientific Background

GABA (γ-aminobutyric acid) is the major inhibitory neurotransmitter in the brain. Its production, release, reuptake, and metabolism all occur in the nervous system.1

The 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.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.2

GABAARs 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

  1. Owens, D.F. and Kriegstein, A.R. (2002) Nat. Rev. Neurosci3, 715.
  2. Whiting, P.J. (1999) Neurochem. Int. 34, 387.
  3. Mihic, S.J. and Harris, R.A. (1997) Alcohol Health Res. World 21, 127.
  4. Neelands, T.R. et al. (1999) J. Neurosci. 197057.
  5. Fuchs, K. and Celepirovic, N. (2002) J. Neurochem82, 1512.
Related Products