Acute blockade of CB1 receptor leads to reinstatement of MDMA-induced conditioned place preference.

Manuel Daza‐losada; José Miñarro; María A. Aguilar; Olga Valverde; Marta Rodríguez‐arias

doi:10.1016/j.pbb.2011.07.011

Acute blockade of CB1 receptor leads to reinstatement of MDMA-induced conditioned place preference.

Manuel Daza‐losada, José Miñarro, María A. Aguilar, Olga Valverde, Marta Rodríguez‐arias

Pharmacology, Biochemistry, and Behavior November 2011 DOI: 10.1016/j.pbb.2011.07.011 (opens in new tab)

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Study at a glance

AI-extracted from the abstract

Characteristics	Experimental study Peer reviewed
Population	Mice
Interventions	MDMA WIN 55 212-2 SR 141716A
Dose	MDMA 5 mg/kg, WIN 55,212-2 0.1 and 0.5 mg/kg, SR 141716A 0.3 mg/kg
Measures	conditioned place preference (CPP)
Topics	MDMA
Key findings	The CB1 antagonist SR 141716A (0.3 mg/kg) alone or with MDMA priming reinstated the MDMA-induced CPP, while the CB1 agonist WIN 55,212-2 had no effect alone but potentiated the effects of subthreshold priming doses of MDMA.

Abstract

Cannabis is one of the drugs most commonly consumed in combination with ecstasy (3,4-methylenedioxymethamphetamine, MDMA). Although numerous studies have attempted to further our understanding of the role of the cannabinoid system in drug abuse, few have focused on how it influences the rewarding effects of MDMA. The aim of the present study was to evaluate the role of the CB1 cannabinoid receptor in vulnerability to reinstatement of a MDMA-induced conditioned place preference (CPP). Mice were first conditioned with 5mg/kg of MDMA. Once the preference had been extinguished, a priming dose of MDMA, alone or plus the CB1 cannabinoid agonist WIN 55,212-2 (0.1 and 0.5mg/kg) or the CB1 cannabinoid antagonist SR 141716A (0.3mg/kg), was administered on alternate days. The CB1 receptor antagonist, alone or with any of the priming doses of MDMA, induced reinstatement of the preference. In contrast, WIN 55,212-2 had no effect on reinstatement of the MDMA-induced CPP when administered alone, but potentiated the effects of subthreshold priming doses of MDMA. These results highlight the important role of the CB1 receptor in vulnerability to reinstatement of drug-seeking behavior and point to the importance of the endocannabinoid system in the addictive potential of MDMA.

Comparable studies

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

Study	Year	Design
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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