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Involvement of D1 dopamine receptor in MDMA-induced locomotor activity and striatal gene expression in mice.

Nadia Benturquia, Cindie Courtin, Florence Noble, Cynthia Marie‐claire

Brain Research May 23, 2008 DOI: 10.1016/j.brainres.2008.03.016 (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Preclinical experimental study in mice Peer reviewed
Population Mice
Interventions MDMA SCH23390
Dose SCH23390 0.05 mg/kg
Topics MDMA
Key findings The D1 receptor antagonist SCH23390 at 0.05 mg/kg completely blocked MDMA-induced locomotor hyperactivity but only partially reduced MDMA-induced increases in Fos, Fosb, Egr1, and Egr2 mRNA (by 24%, 23%, 22%, and 29%, respectively). The authors conclude that D1 receptors play a key role in acute MDMA-induced hyperlocomotion and that ERK-dependent immediate-early gene transcription is only partially under D1 receptor control.

Abstract

3,4-Methylenedioxymethamphetamine (MDMA), a widely used recreational drug with psychoactive properties, induces both serotonin and dopamine release in the brain. In rats and mice MDMA induces behavioural changes and has rewarding effects but little is known about its cellular effects. We have previously shown that the ERK pathway is important for the changes in gene expression observed in mice striatum after treatment with this psychostimulant. In this study we investigated the role of D1 receptors in MDMA-induced locomotor hyperactivity and regulation of immediate-early genes (Fos, Fosb, Egr1 and Egr2) mRNA levels requiring ERK activity in mice striatum. We used the selective D1 receptor antagonist, SCH23390 at a dose (0.05 mg/kg) that did not influence locomotor activity. This dose totally blocked MDMA-induced locomotor activity but only partially the increase in transcription levels of Fos, Fosb, Egr1 and Egr2 (24%, 23%, 22% and 29% respectively). In conclusion, our results showed that D1 receptors play a key role in the acute MDMA-induced hyperlocomotion and that ERK pathway is partially under D1 receptors control to induce Fos, FosB, Egr1 and Egr2 transcription.

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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