Gamma-aminobutyric acid (GABA) is a potent amino acid neurotransmitter with various physiologic effects throughout the body. Over the past 40 years it has become evident that the mammalian liver contains high concentrations of GABA which are carefully regulated by a series of hepatic metabolic pathways and a specific sodium-dependent active transport system. It is also clear that the liver possesses sodium-independent, bicuculline-sensitive GABAA receptor sites which when innervated cause marked hyperpolarization of the hepatocyte transmembrane potential. Recent data suggest that extensive hepatic injury alters GABA homeostatic mechanisms which in turn may contribute to the pathogenesis of hepatic encephalopathy and systemic hypotension. There is also reason to believe that increased GABAergic activity may inhibit hepatic regeneration following partial hepatectomy in rats.