Tissue distribution, metabolism and effects of bufotenine administered to rats.

Bufotenine, a serotonin analog, was injected into rats at doses of 1, 30, or 100 mg/kg. One hour later, concentrations were highest in lung, heart, and blood, and lower in brain and liver. Bufotenine was nearly gone by 8 hours. It was slightly higher in hypothalamus and brain stem than in striatum or cortex; serotonin decreased slightly while its metabolite 5HIAA increased in those regions. Type A monoamine oxidase, not type B, metabolizes bufotenine. Bufotenine raised serum corticosterone, an effect not blocked by metergoline. Over 99% of bufotenine was in platelet-poor plasma, indicating it is not stored in platelets. Bufotenine penetrates the blood-brain barrier poorly and is rapidly eliminated.

Study at a glance

Abstract

Bufotenine (N, N-dimethyl-5-hydroxytryptamine) is a serotonin analog reported to be hallucinogenic. Bufotenine concentrations were measured by liquid chromatography with electrochemical detection after the s.c. injection of bufotenine (1, 30 or 100 mg/kg) into rats. At 1 hr, bufotenine was high in lung, heart and blood and lower in brain and liver. No N-monomethyl-5-hydroxytryptamine was detected, but 5-hydroxyindoleacetic acid (5HIAA) was increased due to bufotenine metabolism. Bufotenine disappeared nearly completely by 8 hr. Bufotenine concentrations were slightly higher in hypothalamus and brain stem than in striatum or cortex; serotonin was slightly decreased, and 5HIAA was increased in these brain regions. Pargyline reduced concentrations of 5HIAA in blood and tissues after bufotenine injection; LY51641 but not deprenyl mimicked pargyline, suggesting type A not type B monoamine oxidase metabolizes bufotenine. Bufotenine injection increased serum corticosterone concentration, an effect not blocked by metergoline at a dose that blocked a similar increase elicited by quipazine. Although only 2% of the serotonin was found in platelet-poor plasma, more than 99% of the bufotenine was found in platelet-poor plasma, indicating that bufotenine is not stored in platelets. These experiments indicate that bufotenine is rapidly eliminated, in part by type A monoamine oxidase, after its injection into rats and that bufotenine penetrates the blood-brain barrier poorly.