Current evidence suggests that anxiety has a neurobiologic basis. It is thought to be caused by dysfunction of one or more neurotransmitters and their receptors. Most data, which are derived from study of the benzodiazepine—γ-aminobutyric acid receptor complex, indicate that alteration of the influx of chloride ions within this receptor complex is associated with the development of anxiety. The primary therapeutic effect of benzodiazepines occurs at this receptor complex. All clinically available benzodiazepines are active at this receptor complex, producing therapeutic results and side effects. Subtypes of benzodiazepine receptors as well as endogenous benzodiazepine ligands also have been identified. These may play a role in the pathogenesis of anxiety. Benzodiazepines also modulate the production of neuroactive steroids in the central nervous system. In the future, drugs that affect these varying benzodiazepine functions may play a role in the treatment of anxiety. Other neurotransmitters also have been implicated in the genesis of anxiety. Drugs affecting the noradrenergic β receptor and the 5-hydroxytryptamine (serotonin) receptors have anxiolytic properties. New evidence also suggests a role for adenosine and cholecystokinin in the development of anxiety; drugs interacting with these neurotransmitters also may have anxiolytic properties.