allnightergl replied: "Buspirone is a psychotropic drug with anxiolytic properties which belongs chemically to the class of compounds known as the azaspirodecanediones. Buspirone shares some of the properties of the benzodiazepines and the neuroleptics, as well as demonstrating other pharmacological action. It attenuates punishment suppressed behavior in animals and exerts a taming effect, but is devoid of anticonvulsant and muscle relaxant properties and does not bind to the benzodiazepine/GABA receptor complex. Buspirone affects a variety of dopamine mediated biochemical and behavioral events, but is free of cataleptic activity. Buspirone has an affinity for brain D(2)-dopamine receptors, where it acts as an antagonist and agonist, and for the 5-HT(1A) receptors, where it acts as an agonist. Buspirone does not block the neuronal reuptake of monoamines and, on chronic administration, it does not lead to changes in receptor density in the models investigated. However, the mechanism of action of buspirone remains to be fully elucidated. Buspirone is rapidly absorbed in man and undergoes extensive first pass metabolism. Following oral administration, low peak plasma levels of unchanged drug, of 1 to 6 ng/mL were observed 40 to 90 minutes after a single 20 mg dose. In a number of studies performed in healthy volunteers, the mean half-life of buspirone ranged from 2 to 3 hours up to approximately 11 hours with considerable variation in individual values. Multiple dose studies suggest that steady state plasma levels were usually achieved within a few days. Buspirone is metabolized primarily by oxidation, producing several hydroxylated derivatives and a pharmacologically active metabolite, 1-pyrimidinylpiperazine (1-PP). Peak plasma levels of 1-PP have been found to be higher than those of its parent drug and its half-life to be approximately double that of unchanged buspirone. In a single dose study using (14)C labeled buspirone, 29 to 63% of the dose was excreted in the urine within 24 hours, primarily as metabolites, while fecal excretion accounted for 18 to 38% of the dose. In man, approximately 95% of buspirone is plasma protein bound, but other highly bound drugs, e.g. phenytoin, propranolol and warfarin, are not displaced by buspirone from plasma protein in vitro. However, in vitro binding studies show that buspirone does displace digoxin. The effect of food upon the bioavailability of buspirone was studied in 8 subjects. The area under the plasma concentration curve (AUC) and peak plasma concentration (C(max)) of unchanged buspirone increased by 84% and 116% respectively when the drug was administered with food, but the total amount of buspirone immunoreactive material did not change. The significance of this finding is not known, but it could indicate that food may decrease the presystemic clearance of buspirone. Buspirone had no effect on hepatic microsomal enzyme activity when administered to rats for 5 days. In man, the effect of buspirone on drug metabolism or concomitant drug disposition has not been studied. The pharmacokinetics of buspirone in patients with hepatic or renal dysfunction, and in the elderly, has also not been clearly established."