AbstractClinical trials have demonstrated that buspirone (BusparTM) is effective in the treatment of anxiety with efficacy and dosage comparable to diazepam or clorazepate. Buspirone is chemically distinct from the benzodiazepines as well as other psychoactive drugs. More importantly, buspirone presents a clinical pharmacologic profile which is “anxioselective”; that is, it relieves anxiety without the accompanying ancillary properties of benzodiazepines (sedation, muscle relaxation, seizure control). Biochemical investigations have not conclusively identified any direct interaction of buspirone with the benzodiazepine‐γ‐aminobutyric acid (GABA)‐chloride ionophore complex. It has been known that buspirone possesses some pharmacologic properties that are shared by dopamine antagonists. However, these properties are not characteristic solely of this class of agents. In contrast to dopamine antagonists, buspirone does not produce catalepsy. In fact, buspirone reverses catalepsy induced by dopamine antagonists. Recent investigations have demonstrated that chronic administration of dopamine antagonists increases dopamine receptor binding in experimental animals. Chronic treatment with buspirone does not have this effect. In conjunction with other observations, it has now become obvious that buspirone does not possess the postsynaptic dopamine antagonism characteristic of antipsychotic drugs. However, the mechanism by which buspirone alleviates the clinical manifestations of anxiety continues to be