About: Bufotenin is a research topic. Over the lifetime, 50 publications have been published within this topic receiving 801 citations. The topic is also known as: 5-OH-DMT & dimethylserotonin.
TL;DR: Preliminary evidence gathered in laboratories from rats infused intraventricularly with bufotenin has suggested that this substance is at least as potent as its powerfully hallucinogenic 5-methoxy congener, and may not easily cross the blood-brain barrier.
Abstract: TANIMUKAI et al.1, using gas-liquid separation, correlated the appearance of a bufotenin-like substance in urine and the onset of psychosis in latent schizophrenics brought on by administration of a monoamine oxidase inhibitor with amino-acid precursors of indoleamines and methyl groups. Serious doubt about endogenous bufotenin as the cause of psychiatric disturbance was cast by research demonstrating that intravenously administered bufotenin produced nothing but bizarre cardiovascular symptoms in man2, 3. One objection to such work is that bufotenin may not easily cross the blood-brain barrier. Recent preliminary evidence gathered in our laboratories from rats infused intraventricularly with bufotenin has suggested that this substance is at least as potent as its powerfully hallucinogenic 5-methoxy congener (unpublished results of D. Segal and A. J. M.).
TL;DR: 5-Methoxytryptamine has been found in the urine of patients with rheumatic fever, and that in an order of magnitude of 30–210 µg/24 h, while N,N-dimethyl-5-hydroxytryptamine was still not demonstrated in blood.
Abstract: TRYPTAMINE is a normal constituent of human urine1–5; about 30–120 µg of the amine are excreted per 24 h. In blood, tryptamine has hitherto been demonstrated only qualitatively and under pathological conditions in a carcinoid patient6. There is no information about an occurrence of N,N-dimethyltryptamine in human beings. N,N-dimethyl-5-hydroxytryptamine (= Bufotenin) was demonstrated qualitatively as a constituent of normal human urine4,7; in children an excretion of 0–0.03 µg amine/100 mg creatinine has been found with, at most, semi-quantitative methods4. Apparently, N,N-dimethyl-5-hydroxytryptamine was still not demonstrated in blood. 5-Methoxytryptamine has been found in the urine of patients with rheumatic fever8, and that in an order of magnitude of 30–210 µg/24 h.
TL;DR: Of many drugs tested, inhibition of specific 3H-serotonin binding occurred almost exclusively with serotonin agonists and antagonists.
Abstract: The specific binding of 3H-serotonin to calf caudate homogenate was studied. The dissociation constant was 2 nM and the number of specific sites was 14 fmoles/mg protein. Of many drugs tested, inhibition of specific 3H-serotonin binding occurred almost exclusively with serotonin agonists and antagonists. The concentrations for 50% inhibition of 3H-serotonin binding by serotonergic agonists follow: bufotenin, 6 nM; 5-methoxytryptamine, 12 nM; psilocin, 35 nM; dimethyltryptamine, 220 nM; and tryptamine, 270 nM. The concentrations for the antagonists were: LSD 9.5 nM; methysergide 16 nM and metergoline 25 nM.
TL;DR: On the basis of their previous work indicating that tryptamine appeared in increased concentrations in the urine before and during the activation of psychotic symptoms, they suggested that under loading conditions the formation of various N,N-dimethylated indoleamines might be facilitated in the body.
Abstract: In addition to tryptamine and serotonin, we found bufotenin (5-hydroxy-N, N-dimethyl-tryptamine) both in free and conjugated forms in the urine of four schizophrenic patients under dietary control when they were receiving tranylcypromine, with or without cysteine loading. The amount of bufotenin was estimated to be as little as 4-10 µg per 24 hr. urine ; one-half in the free, one-half in the conjugated form. In the absence of monoamine oxidase blockade bufotenin was also excreted in some patients, but less than 1 µg per day.
N-methylserotonin, N, N-dimethyltryptamine and 5-methoxy-N, N-dimethyltryptamine were also disclosed, but only by thin-layer chromatography and especially when the patients were receiving tranylcypromine with or without cysteine. Increases of urinary bufotenin and other N-methylated indoleamines were observed about two weeks before the mental and behavioural symptoms of the schizophrenic patients worsened, and these elevated levels continued during the period of behavioural exacerbations.