6533b829fe1ef96bd1289844

RESEARCH PRODUCT

Role of AMPA glutamate receptors in the conditioned rewarding effects of MDMA in mice

María A. AguilarMaría Pilar García-pardoMaría Pilar García-pardoJosé Miñarro

subject

MaleHallucinogenMDMAmiceN-Methyl-34-methylenedioxyamphetamineAmphetamine-Related DisordersSpatial BehaviorKainate receptorAMPA receptorPharmacologyMice03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compound0302 clinical medicineRewardConditioning Psychologicalmental disordersmedicineAnimalsReceptors AMPAAMPA receptorsreward6-Cyano-7-nitroquinoxaline-23-dioneDose-Response Relationship Drugbusiness.industryGlutamate receptorMDMACNQXconditioned place preferenceConditioned place preference030227 psychiatrynervous systemchemistryHallucinogensCNQXNMDA receptorbusinessExcitatory Amino Acid Antagonistspsychological phenomena and processes030217 neurology & neurosurgerymedicine.drug

description

Abstract Currently, there is not an effective treatment for 3,4-methylenedioxymethamphetamine (MDMA) dependence but pharmacotherapies targeting glutamate neurotransmission are a promising strategy. Previously, we showed that blockade of glutamate NMDA and AMPA receptors impairs the conditioned rewarding effects of MDMA and cocaine, respectively. In this study we evaluated the role of AMPA receptors in the rewarding effects of MDMA in mice using the conditioned place preference (CPP) paradigm. Mice were conditioned with MDMA (1.25 mg/kg) 60 min after the treatment with saline or different doses (0.25, 1 and 5 mg/kg) of the AMPA/kainate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Mice conditioned with MDMA acquired CPP while those treated with any dose of CNQX + MDMA did not. These results supported the involvement of the glutamatergic system in the rewarding properties of MDMA, and suggest that AMPA receptor blockade could be a new therapeutic option for the treatment of those individuals that develop MDMA dependence.

yearjournalcountryeditionlanguage
2018-07-01Behavioural Brain Research
https://doi.org/10.1016/j.bbr.2018.03.010