Abstract
Summary
Normal rat brain tryptamine concentration was 0.032 ± 0.002 μg/g (mean ± S.E.M.). Oral administration of 0.72 mg/ kg of tranylcypromine (trans 2-phenylcyclopropylamine) or 25 mg/kg of iproniazid (1-isonicotinyl-2-isopropyl hydrazine) had no apparent effect upon normal rat brain tryptamine concentration. Sixty to 75 seconds after i.v. injection of non-convulsive dose of tryptamine (5 mg/kg) brain concentration of the amine was increased to 0.173 ± 0.019 μg/ g. Occurrence, duration and relative intensity of clonic convulsions produced by injection of tryptamine into rats pretreated with either of above monoamine oxidase inhibitors were correlated with increased concentration of amine in the rat brain. In view of demonstrated ability of systemically injected tryptamine to penetrate rat brain, it is reasonable to conclude that the elicited pharmacologic effects reflected a central mechanism of action of the amine, potentiated by inhibition of brain monoamine oxidase activity.
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