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Behavioral effects and metabolic fate of N,N-dimethyltryptamine in mice pretreated with beta-diethylaminoethyl-diphenylpropylacetate (SKF 525-A), improniazid and chlorpromazine.

N S Shah, M P Hedden

Pharmacology, Biochemistry, and Behavior April 1978 DOI: 10.1016/0091-3057(78)90070-9 (opens in new tab)

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Characteristics Animal experimental study Peer reviewed
Population Mice
Interventions N N-dimethyltryptamine (DMT) iproniazid SKF 525-A chlorpromazine
Dose DMT 2.5, 10.0, and 25.0 mg/kg; iproniazid 153 mg/kg; SKF 525-A 50 mg/kg; chlorpromazine 15 mg/kg
Duration Iproniazid 4 hr; SKF 525-A 1 hr; chlorpromazine 0.5 hr before DMT
Topics 5-MeO-DMT DMT
Key findings DMT produced dose-related behavioral changes in mice that generally coincided with brain DMT concentrations. Iproniazid, a monoamine oxidase inhibitor, prolonged and enhanced DMT's behavioral and tissue effects, whereas SKF 525-A did not and chlorpromazine abolished responses to 25 mg/kg. The authors conclude that DMT is metabolized chiefly by monoamine oxidase rather than hepatic microsomal enzymes, and that its behavioral effects are due to the parent compound rather than a metabolite.

Abstract

Behavioral aspects and metabolic fate of N,N-dimethyltryptamine (DMT) were studied in mice pretreated with beta-diethylaminoethyl-diphenylpropylacetate (SKF 525-A), iproniazid or chlorpromazine (CPZ). DMT at doses of 2.5, 10.0, and 25.0 mg/kg produced several behavioral changes in a dose-related manner: inhibition of spontaneous locomotor movement, enhanced fright responses to sound stimuli, trembling, head twitching, inco-ordinated movements of hind-legs, flat or extended tail and abnormal posture with the extension of hind-legs. Pretreatment with ipromazid (153 mg/kg; 4 hr) but not SKF 525-A (50 mg/kg; 1 hr) prolonged the behavioral effects produced by 2.5 mg/kg DMT while CPZ (15 mg/kg; 0.5 hr) completely abolished the responses induced by 25 mg/kg DMT. Earlier behavioral effects generally coincided with the brain concentrations of DMT. Dose-dependent increases with rapid uptake and disappearance in the brain, plasma and hepatic levels of DMT were measured with doses of 10 and 25 mg/kg DMT. Iproniazid but not SKF 525-A markedly enhanced tissue levels of DMT. it is concluded that DMT is metabolized chiefly by monoamine oxidase rather than by drug-metabolizing hepatic microsomal enzymes and that DMT-induced behavioral effects are due to the parent compound rather than its metabolite.

Comparable studies

Other preclinical and animal studies on 5-MeO-DMT, most cited first.

Study Year Design Participants
Psychedelic N,N-dimethyltryptamine and 5-methoxy-N,N-dimethyltryptamine modulate innate and adaptive inflammatory responses through the sigma-1 receptor of human monocyte-derived dendritic cells. Human primary monocyte-derived dendritic cells 2014 In vitro study
Effects of N,N-Dimethyltryptamine on Rat Behaviors Relevant to Anxiety and Depression Adult male Sprague-Dawley rats 2018 Experimental study
Hallucinogen-like actions of 5-methoxy-N,N-diisopropyltryptamine in mice and rats. Mice and rats 2006 Preclinical study
Agonist Properties of N,N-Dimethyltryptamine at Serotonin 5-HT2A and 5-HT2C Receptors Rats and transfected fibroblasts 1998 Experimental study
Subtypes of the 5-HT receptor mediating the behavioural responses to 5-methoxy-N,N-dimethyltryptamine in the rat Intact rats and rats depleted of monoamines with reserpine 1985 Experimental study

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