Effect of alpha-alkylated tryptamine derivatives on 5-hydroxytryptamine metabolism in vivo.
In rats, three alpha-alkylated tryptamine derivatives (alpha-methyl, alpha-ethyl, and alphaalpha-dimethyltryptamine) caused alterations of 5-hydroxytryptamine metabolism typical of monoamine-oxidase inhibitors with short duration of action, viz., an increase of endogenous 5-hydroxytryptamine in brain, enhancement of the increase of 5-hydroxytryptamine in brain and heart after 5-hydroxytryptophan administration, an inhibition of the decrease in 5-hydroxytryptamine in brain induced by a benzoquinolizine derivative and of the increase induced by iproniazid. The increase after iproniazid was antagonized to the same extent by all the tryptamine derivatives and by harmaline, whereas dexamphetamine showed less effect. In the other experiments with brain, the tryptamine derivatives were less potent than harmaline, but somewhat more active than dexamphetamine. alpha-Methyltryptamine and alpha-ethyltryptamine were relatively more effective in the heart than in the brain. Among the tryptamine derivatives alphaalpha-dimethyltryptamine had the weakest activity in brain and in heart.
K F
KF
GEY
A
A
PLETSCHER
D006916:5-Hydroxytryptophan; D000818:Animals; D001921:Brain; D007490:Iproniazid; D008996:Monoamine Oxidase Inhibitors; D004130:N,N-Dimethyltryptamine; D051381:Rats; D012701:Serotonin / Q000378:metabolism*; D014363:Tryptamines
D008996:Monoamine Oxidase Inhibitors; D014363:Tryptamines; D012701:Serotonin; C030820:tryptamine; C015293:indopan; D006916:5-Hydroxytryptophan; D007490:Iproniazid; C038034:etryptamine; D004130:N,N-Dimethyltryptamine
SEROTONIN/metabolism