The A-type receptors for γ-aminobutyric acid (GABA(A)) mediate the majority of fast inhibitory transmission in the mammalian central nervous system. Many clinically important drugs including benzodiazepines, barbiturates and general anesthetics act as positive allosteric modulators of this receptor¹. GABA(A) receptors are pentameric ligand-gated ion-channels, composed of subunits from many subunit classes: α1-α6, β1-β4, γ1-γ4, δ, ε , θ, π and ρ1-ρ3².  The arrangement of subunits around the channel is probably γβαβα counter-clockwise when viewed from the extracellular space, ε and π subunits can replace the γ and δ subunit within the pentamer, whereas the θ subunit could replace a β subunit³.

The localized expression of this subunit is consistent with the fact that all GABA(A) receptor subunit genes have distinct expression patterns in the brain³. The θ subunit has been reported to be strongly expressed in the striatum and has been localized to the locus ceruleus⁴.

Impairment of the γ-aminobutyric acid (GABA) signaling system is believed to partially account for behavioral and cognitive deficits associated with schizophrenia and mood disorders⁵. Reduction of GABA(A) mediated signal transmission has also been associated with anxiety, panic, impaired learning and memory⁶.