Effect of Some Indolealkylamines on Man

Turner, William J.; Merlis, Sidney

doi:10.1001/archneurpsyc.1959.02340130141020

Cited by 83 publications

(36 citation statements)

References 16 publications

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“…Smoked DMT effects are extremely intense (Strassman, 2001; Turner, 1994). Intranasal free-base DMT was inactive (0.07 – 0.28 mg/kg; Turner and Merlis, 1959) as was DMT administered rectally as 1.7 mg/kg of the bioxalate salt (de Smet, 1983). …”

Section: Pharmacokinetics Of Dmtmentioning

confidence: 99%

Neuropharmacology of N,N-dimethyltryptamine

Carbonaro

Gatch

2016

Brain Research Bulletin

171

169

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N,N-Dimethyltryptamine (DMT) is an indole alkaloid widely found in plants and animals. It is best known for producing brief and intense psychedelic effects when ingested. Increasing evidence suggests that endogenous DMT plays important roles for a number of processes in the periphery and central nervous system, and may act as a neurotransmitter. This paper reviews the current literature of both the recreational use of DMT and its potential roles as an endogenous neurotransmitter. Pharmacokinetics, mechanisms of action in the periphery and central nervous system, clinical uses and adverse effects are also reviewed. DMT appears to have limited neurotoxicity and other adverse effects except for intense cardiovascular effects when administered intravenously in large doses. Because of its role in nervous system signaling, DMT may be a useful experimental tool in exploring how brain works, and may also be a useful clinical tool for treatment of anxiety and psychosis.

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Section: Pharmacokinetics Of Dmtmentioning

confidence: 99%

Neuropharmacology of N,N-dimethyltryptamine

Carbonaro

Gatch

2016

Brain Research Bulletin

171

169

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“…There are some doubts about the psychotomimetic activity of bufotenine (Fabing & Hawkins, 1956;Turner & Merlis, 1959) which may be related to the relatively low penetration of the drug into the brain (Sanders & Bush, 1967). However, it has been reported that bufotenine is at least as active as 5-MeODMT in certain animal behaviour tests when it is administered by intraventricular infusion, thus bypassing the blood brain barrier (Mandell, Buckingham & Segal, 1971).…”

Section: Introductionmentioning

confidence: 99%

Further Studies on the Mode of Action of Psychotomimetic Drugs: Antagonism of the Excitatory Actions of 5‐hydroxytryptamine by Methylated Derivatives of Tryptamine

Bradley

Briggs

1974

British J Pharmacology

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1The actions of 5-methoxytryptamine (5-MeOT), N,N-dimethyltryptamine (DMT), 5-hydroxy-N,N-dimethyltryptamine (bufotenine, 5-HODMT) and 5-methoxy-N,Ndimethyltryptamine (5-MeODMT), and their interactions with 5-hydroxytryptamine (5-HT), acetylcholine, (-)-noradrenaline, and glutamate were studied by microiontophoresis on single neurones in the brain stem of rats anaesthetized with urethane or decerebrate cats. 2 Like D-lysergic acid diethylamide (LSD 25) the three psychotomimetic derivatives (DMT, 5-HODMT, 5-MeODMT) specifically antagonized 5-HT excitations of single neurones, but the non-psychotomimetic 5-MeOT had no antagonistic effects. 3 In contrast to LSD 25, the psychotomimetic tryptamines only rarely antagonized glutamate effects, indicating that the excitatory 5-HT receptors and the glutamate receptors on the same neurones may be closely related spatially, but are separate. 4 The methylated tryptamine derivatives were able to mimic the actions of 5-HT on neurones. The non-psychotomimetic 5-MeOT was most potent in this respect, while the other three derivatives which are psychotomimetic, were less active. 5 The 5-HT mimicking actions of 5-MeOT were the same in rats pretreated with p-chlorophenylalanine or reserpine as in untreated rats. It therefore seems that the 5-HT mimicking actions are unlikely to be due to release of 5-HT, but are due to direct actions on 5-HT receptors. 6 The evidence presented supports the hypothesis that LSD-like psychotomimetics act by an antagonism of 5-HT in the lower brain stem, and is not compatible with the suggestion that the psychotomimetic action of these drugs is related to 5-HT receptor stimulation.

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“…The leaves of the admixture plants, which are required for the psychoactive effects of ayahuasca, contain the hallucinogens N,N -dimethyltryptamine (DMT) and 5-methoxy-DMT (5-MeO-DMT) (Agurell et al 1968; Rivier and Lindgren 1972; McKenna et al 1984). DMT is active by parenteral administration or if smoked (Strassman et al 1994; Shulgin and Shulgin 1997), but is inactive orally due to substantial first-pass metabolism (Szára 1957; Turner and Merlis 1959). Agurell et al (1968) first proposed that a specific interaction between β-carbolines and DMT contributes to the oral pharmacological activity of ayahuasca.…”

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confidence: 99%

Modification of the effects of 5-methoxy-N,N-dimethyltryptamine on exploratory behavior in rats by monoamine oxidase inhibitors

et al. 2008

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RATIONALE The hallucinogenic tea known as ayahuasca is made from a combination of psychoactive plants that contribute the active components N,N-dimethyltryptamine (DMT) and 5-methoxy-DMT (5-MeO-DMT), as well as the monoamine oxidase (MAO) inhibitors (MAOIs) harmine and harmaline for oral activity. OBJECTIVE The present study examined the effects of 5-MeO-DMT in combination with MAOIs in rats using the Behavioral Pattern Monitor (BPM), which enables analyses of patterns of locomotor activity and exploration. Interaction studies using the serotonin (5-HT)1A antagonist WAY-100635 (1.0 mg/kg) and the 5-HT2A antagonist MDL 11,939 (1.0 mg/kg) were also performed to assess the respective contributions of these receptors to the behavioral effects of 5-MeO-DMT in MAOI-treated animals. RESULTS 5-MeO-DMT (0.01, 0.1, and 1.0 mg/kg) decreased locomotor activity and investigatory behavior. In rats pretreated with a behaviorally inactive dose of harmaline (0.1 mg/kg), 1.0 mg/kg 5-MeO-DMT had biphasic effects on locomotor activity, initially reducing locomotion and then increasing activity as time progressed. The ability of harmaline to shift 5-MeO-DMT to a biphasic locomotor pattern was shared by the selective MAOA inhibitor clorgyline, whereas the selective MAOB inhibitor (−)-deprenyl was ineffective. The late hyperactivity induced by the combination of 1.0 mg/kg 5-MeO-DMT and 0.3 mg/kg clorgyline was blocked by pretreatment with MDL 11,939. Pretreatment with WAY-100635 failed to attenuate either the early hypoactivity or the late hyperactivity. CONCLUSIONS The ability of harmaline to modify the behavioral effects of 5-MeO-DMT is mediated by inhibition of MAOA. Further, 5-HT2A receptors are responsible for the late hyperactivity induced by 5-MeO-DMT in the presence of MAOA inhibitors.

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Effect of Some Indolealkylamines on Man

Cited by 83 publications

References 16 publications

Neuropharmacology of N,N-dimethyltryptamine

Neuropharmacology of N,N-dimethyltryptamine

Further Studies on the Mode of Action of Psychotomimetic Drugs: Antagonism of the Excitatory Actions of 5‐hydroxytryptamine by Methylated Derivatives of Tryptamine

Modification of the effects of 5-methoxy-N,N-dimethyltryptamine on exploratory behavior in rats by monoamine oxidase inhibitors

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