Every lot is tried & tested in a relevant biological assay.
- Horne, A.L. et al. (1992) Br. J. Pharmacol. 107, 732.
- Alomone Labs γ-Aminobutyric acid reversibley activates GABA(A) α2/β1/γ2 currents heterologously expressed in Xenopus oocytes.Time course activation of GABA(A) α2/β1/γ2 currents by decreasing concentrations (between 1 µM and 1 mM, as indicated) of γ-Aminobutyric acid (#G-110). Holding membrane potential was -60 mV and γ-Aminobutyric acid was applied every 100 seconds as indicated by arrows.
γ-aminobutyric acid (GABA) is an amino acid derivate, synthesized from glutamate by the pyridoxal-L-phosphate (PLP)-dependent enzyme, glutamate decarboxylase (GAD)1. GABA provides the primary inhibitory signaling in the adult mammalian brain (CNS), and, to some degree of controversy, exerts a depolarizing response in the developing brain2.
GABA is an agonist of two main receptor classes in the CNS: GABAA, an ionic ligand gated channel, and GABAB, a metabotrophic, G-protein coupled receptor. GABAA is assembled by 5 out of 16 possible subunits with α, β and either a γ or a δ (2:2:1 stoichiometry) being the most common. With an EC50 between 3 - 12μM it interacts with GABA to allow either an influx or an efflux of Cl- ions, into and out of the cell, respectively3. GABAB is a heterodimer comprised of the subunits GABAB1 and GABAB2. It reduces neurotransmitter release by inhibiting Ca2+ channels when activated presynaptically, and facilitates inward rectifying potassium channels, postsynaptically1.
GABA deficiency is often the prime cause for epilepsy, with other notably disorders being autism4, spasticity, anxiety disorders, schizophrenia, and stiff-person syndrome5.