Benzodiazepines (BZs) produce most, if not all, of their pharmacological actions by specifically enhancing the effects of endogenous and exogenous GABA that are mediated by GABAA receptors. This potentiation consists in an increase of the apparent affinity of GABA for increasing chloride conductance without increase in its efficacy and, on the single chloride channel level, seems to be the result of an increased probability of channel opening events. Recent studies indicate that the BZR is a site on the GABA receptor (GABA-R)-chloride channel complex, through which the gain of the signal transducer function of the latter is allosterically modulated. The unique feature of this drug receptor, which is located on a neurotransmitter receptor-gated ion channel, is its specific interaction with three classes of ligands. Agonists, competitive antagonists and inverse agonists at BZR, respectively increase, do not alter and reduce the gain of the GABA-R function. Compounds have been found that cover a whole spectrum of transition between the two extremes (partial agonists, partial inverse agonists) and for which interesting therapeutic applications can be foreseen.