The development of anxioselective agents has made it possible to examine the biochemical basis of anxiety. Electrophysiological analysis revealed that benzodiazepines selectively enhance gamma-aminobutyric acid (GABA) neurotransmission. Subsequent work demonstrated the presence of a specific population of benzodiazepine binding sites on neuronal membranes. These sites appear to be linked to certain GABA receptors such that occupation of the benzodiazepine component reveals a group of GABA recognition sites that may be more sensitive to the neurotransmitter. These data, coupled with the findings that barbiturates may act, at least in part, by interacting with the GABA receptor-coupled chloride channel, suggest that pharmacological manipulations of the GABA system can alleviate the symptoms of anxiety. The anxioselectivity of the benzodiazepines may be related to the fact that they activate only a certain population of GABA receptors, whereas barbiturates can potentiate the majority of these sites. These discoveries point to the possibility that alterations in the GABA system may partially explain the neurochemical basis of anxiety.