The neurotransmitter GABA (γ-aminobutiric acid) inhibits the activity of signal-receiving neurons by interacting with the GABA_A receptor on these cells.¹ Binding of GABA to its GABA_A receptor results in conformational changes that open a Cl^- channel, producing an increase in membrane conductance that results in inhibition of neural activity.²

There are two major types of GABA receptors: the ionotropic GABA_A receptors (GABA_AR) and the metabotropic GABA_B receptors (GABA_BR). GABA_ARs belong to the ligand-gated ion channel superfamily.^1,2

GABA_ARs are heteropentamers, in which all five subunits contribute to formation of the pore. Eight subunit isoforms have been cloned: α, β, γ, δ, ε, π, θ, and ρ.¹ Six α subunits isoforms (α1-α6) have been shown to exist in mammals.
In most cases, the native GABA_A receptors consist of 2α, 2β, and 1γ subunits. 

The α3-subunit is highly expressed during development (along with α2 and α5) and then declines in adulthood, where the α1-subunit becomes predominant. The failure to complete this switch could be a major predispositional factor in the development of temporal lobe epilepsy.³