Many of alcohol’s effects—subjective, soporific, anxiolytic, and motor-skill impairing, among others—are mediated by activity involving γ -aminobutyric acid (GABA), the neurotransmitter principally responsible for inhibitory neurotransmission in the central nervous system (Kumar, 2009). In particular, ethanol’s action is largely effected, both directly and indirectly, upon type A GABA (GABAA) receptors to mediate many of its behavioral consequences. The subunit composition of a GABAA receptor affects the nature and sensitivity of its response to ethanol exposure, and functional variation in GABAA receptor subunit genes can alter physiological and behavioral response to alcohol and other GABA-active drugs (Lobo and Harris, 2008).
