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Acutely applied MDMA enhances long-term potentiation in rat hippocampus involving D1/D5 and 5-HT2 receptors through a polysynaptic mechanism

dc.contributor.authorRozas C.
dc.contributor.authorLoyola S.
dc.contributor.authorUgarte G.
dc.contributor.authorZeise M.L.
dc.contributor.authorReyes-Parada M.
dc.contributor.authorPancetti F.
dc.contributor.authorRojas P.
dc.contributor.authorMorales B.
dc.date.accessioned2020-09-02T22:27:30Z
dc.date.available2020-09-02T22:27:30Z
dc.date.issued2012
dc.identifier10.1016/j.euroneuro.2011.11.010
dc.identifier.citation22, 8, 584-595
dc.identifier.issn0924977X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6095
dc.description3,4-Methylenedioxymethamphetamine (MDMA, ecstasy) is a drug of abuse that induces learning and memory deficit. However, there are no experimental data that correlate the behavioral evidence with models of synaptic plasticity such as long-term potentiation (LTP) or long-term depression (LTD). Using field potential recordings in rat hippocampal slices of young rats, we found that acute application of MDMA enhances LTP in CA3-CA1 synapses without affecting LTD. Using specific antagonists and paired-pulse facilitation protocols we observed that the MDMA-dependent increase of LTP involves presynaptic 5-HT2 serotonin receptors and postsynaptic D1/D5 dopamine receptors. In addition, the inhibition of PKA suppresses the MDMA-dependent increase in LTP, suggesting that dopamine receptor agonism activates cAMP-dependent intracellular pathways. We propose that MDMA exerts its LTP-altering effect involving a polysynaptic interaction between serotonergic and dopaminergic systems in hippocampal synapses. Our results are compatible with the view that the alterations in hippocampal LTP could be responsible for MDMA-dependent cognitive deficits observed in humans and animals. © 2011 Elsevier B.V. and ECNP.
dc.language.isoen
dc.subject5-HT
dc.subjectDA
dc.subjectHippocampus
dc.subjectLTD
dc.subjectLTP
dc.subjectMDMA
dc.subject3,4 methylenedioxymethamphetamine
dc.subject8 chloro 2,3,4,5 tetrahydro 3 methyl 5 phenyl 1h 3 benzazepin 7 ol hydrogen maleate
dc.subjectcyclic AMP
dc.subjectcyclic AMP dependent protein kinase
dc.subjectcyclic AMP dependent protein kinase inhibitor
dc.subjectdopamine 1 receptor
dc.subjectdopamine 5 receptor
dc.subjectketanserin
dc.subjectserotonin 2 receptor
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectarticle
dc.subjectcontrolled study
dc.subjectdopaminergic system
dc.subjectdrug effect
dc.subjectenzyme inhibition
dc.subjecthippocampus
dc.subjectlong term depression
dc.subjectlong term potentiation
dc.subjectnerve cell plasticity
dc.subjectnerve stimulation
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectrat
dc.subjectserotoninergic system
dc.subjectsynapse
dc.subjectAnimals
dc.subjectCyclic AMP-Dependent Protein Kinases
dc.subjectDopamine Antagonists
dc.subjectEnzyme Activation
dc.subjectEvoked Potentials
dc.subjectHallucinogens
dc.subjectHippocampus
dc.subjectLong-Term Potentiation
dc.subjectN-Methyl-3,4-methylenedioxyamphetamine
dc.subjectNerve Tissue Proteins
dc.subjectNeurons
dc.subjectPresynaptic Terminals
dc.subjectProtein Kinase Inhibitors
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectReceptors, Dopamine
dc.subjectReceptors, Dopamine D1
dc.subjectReceptors, Dopamine D5
dc.subjectReceptors, Serotonin, 5-HT2
dc.subjectSerotonin 5-HT2 Receptor Antagonists
dc.subjectSerotonin Agents
dc.subjectSynaptic Transmission
dc.titleAcutely applied MDMA enhances long-term potentiation in rat hippocampus involving D1/D5 and 5-HT2 receptors through a polysynaptic mechanism
dc.typeArticle


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