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Adolescent pre‐exposure to ethanol and 3,4‐methylenedioxymethylamphetamine (MDMA) increases conditioned rewarding effects of MDMA and drug‐induced reinstatement

Bruno Ribeiro Do Couto, Manuel Daza‐losada, Marta Rodrı́guez-arias, Roser Nadal, Consuelo Guerri, Teresa Summavielle, José Miñarro, María A. Aguilar

Addiction Biology October 13, 2011 DOI: 10.1111/j.1369-1600.2011.00382.x (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Animal study Peer reviewed
Population Adolescent mice
Interventions Ethanol MDMA
Dose 2 g/kg EtOH, 10 or 20 mg/kg MDMA
Topics MDMA Serotonin
Keywords Conditioned place preference Dopamine Pharmacology Conditioning Ethanol Methamphetamine Hallucinogen Extinction optical mineralogy Biochemistry
Citations 26
Key points Pre-exposure to ethanol or MDMA during adolescence increased the rewarding effects and persistence of MDMA-induced conditioned place preference, and lowered the threshold for reinstatement.

Abstract

ABSTRACT Many adolescents often take ethanol (EtOH) in combination with 3,4‐methylenedioxymethylamphetamine (MDMA). In the present work, we used a mouse model to study the effect of repeated pre‐exposure during adolescence to EtOH (2 g/kg), MDMA (10 or 20 mg/kg) or EtOH + MDMA on the rewarding and reinstating effects of MDMA in the conditioned place preference (CPP) paradigm. Pre‐exposure to EtOH, MDMA or both increased the rewarding effects of a low dose of MDMA (1.25 mg/kg). These pre‐treatments did not affect the acquisition of the CPP induced by 5 mg/kg of MDMA. However, the CPP was more persistent in mice pre‐exposed to both doses of MDMA or to EtOH + MDMA20. After extinction of the CPP induced by 5 mg/kg of MDMA, reinstatement was observed in all groups with a priming dose of 2.5 mg/kg of MDMA, in the groups pre‐exposed to EtOH or MDMA alone with a priming dose of 1.25 mg/kg, and in the groups pre‐treated with MDMA alone with a priming dose of 0.625 mg/kg. Pre‐treatment during adolescence with MDMA or EtOH induced long‐term changes in the level of biogenic amines [dihydroxyphenyl acetic acid, homovanillic acid, dopamine turnover, serotonin (5‐hydroxytryptamine, 5‐HT) and 5‐hydroxyindole acetic acid (5‐HIAA) in the striatum, and 5‐HT and 5‐HIAA in the cortex] after the first reinstatement test, although these effects depended on the dose used during conditioning. These results suggest that exposure to EtOH and MDMA during adolescence reinforces the addictive properties of MDMA.

Comparable studies

Other preclinical and animal studies on MDMA, most cited first.

Study Year Design Participants
Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Rats (implied by typical neurochemical study context) 1987 Experimental study
3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Rat brain 1987 Animal experiment
Comparison of the monoamine transporters from human and mouse in their sensitivities to psychostimulant drugs Human and mouse dopamine, norepinephrine, and serotonin transporters expressed in cells 2006 In vitro laboratory study
Small Changes in Ambient Temperature Cause Large Changes in 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonin Neurotoxicity and Core Body Temperature in the Rat Rats 1998 Experimental study
Altered Serotonin Innervation Patterns in the Forebrain of Monkeys Treated with (±)3,4-Methylenedioxymethamphetamine Seven Years Previously: Factors Influencing Abnormal Recovery Squirrel monkeys treated with MDMA 1999 Observational cohort

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MDMA Serotonin Addiction