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: GABA_A, an ionic ligand-gated channel, and GABA_B, a metabotrophic, G-protein coupled receptor. GABA_A 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 to 12 μM it interacts with GABA to allow either an influx or an efflux of Cl^- ions into and out of the cell, respectively³.

Bicuculline (BIC) is a competitive allosteric inhibitor of GABA_A-induced currents with an IC₅₀ of 1-3 μM⁴. BIC has been employed to model epileptic seizures in hippocampal slices⁵, to induce schizophrenia-like symptoms in the pre-frontal cortex⁶, and is an essential research tool in the study of various psychomotor and behavioral defects^4-6.