Rapid synaptic inhibition is mediated through GABAA receptors that are ligand-gated, chloride ion channels. GABAB receptors are G protein-coupled receptors that are present in almost all CNS neurons and regulate synaptic transmission and signal propagation. A substantial body of evidence from preclinical studies has implicated GABAA receptors in the acute and chronic effects of ethanol including tolerance, dependence and withdrawal [14]–[16]. Preclinical studies have implicated GABAB receptors in the rewarding effects of drugs of abuse [17], [18]. Indeed, GABAB agonists have been found to decrease alcohol consumption and craving in humans and severity of alcohol withdrawal symptoms in humans and rats [17], [19].
