Buspirone: An Update on a Unique Anxiolytic Agent

Buspirone (Buspar) is a azaspirodecanedione anxiolytic agent. Its mechanism of action is extremely complex, but current investigations indicate that its main neuropharmacologic effects are mediated by the 5‐HT_1A receptors. Other neuroreceptor systems could be involved, as buspirone displays some affinity for DA₂ autoreceptors and 5‐HT₂ receptors. It has been proposed that inhibition of synthesis and release of serotonin result through the combined interactions of neuroreceptors and secondary messenger systems. This action leads to inhibition of the firing rate of 5‐HT‐containing neurons in the dorsal raphe. From this novel profile, that differs from that of the benzodiazepines, buspirone lacks anticonvulsant and muscle‐relaxant properties, and causes only mimimal sedation. The drug is rapidly absorbed after oral administration, with a mean bioavailability of 3.9%. After a single oral dose, the mean elimination half‐life is 2.1 hours. Buspirone is mainly bound to albumin and oxacid glycoprotein. It is metabolized to an active metabolite 1‐(2‐pyrimidinyl) piperazine (1‐PP). The mean elimination half‐life of 1‐PP is 6.1 hours. Buspirone is indicated in the treatment of generalized anxiety disorders. Its efficacy is comparable to the benzodiazepines. Its use in depression and panic disorders requires further investigation. When combined with alcohol or given alone, psychomotor impairment was not detected. Abuse, dependence, and withdrawal symptoms have not been reported. The frequency of adverse effects is low, and the most common effects are headaches, dizziness, nervousness, and lightheadness. Buspirone should be added to drug formularies and could represent a significant addition in psychopharmacology. 1988 Pharmacotherapy Publications Inc.