For almost three decades now, the GABAergic synapse has been the focus of intense study for its putative role in mediating many of the behavioral consequences associated with acute and chronic ethanol exposure. Although it was initially thought that ethanol interacted solely with the postsynaptic GABAA receptors that mediate the majority of fast synaptic inhibition in the mammalian central nervous system (CNS), a number of recent studies have identified novel pre- and postsynaptic mechanisms that may contribute to the acute and long-term effects of ethanol on GABAergic synaptic inhibition. These mechanisms appear to differ in a brain region specific manner and may also be influenced by a variety of endogenous neuromodulatory factors. This article provides a focused review of recent evidence, primarily from in vitro brain slice electrophysiological studies, that offers new insight into the mechanisms through which acute and chronic ethanol exposures modulate the activity of GABAergic synapses. The implications of these new mechanistic insights to our understanding of the behavioral and cognitive effects of ethanol are also discussed.