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Bidirectional Hebbian plasticity at hippocampal mossy fiber synapses on CA3 interneurons

dc.creatorGalván, Emilio J.
dc.creatorCalixto, Eduardo
dc.creatorBarrionuevo, Germán
dc.date.accessioned2017-06-29T06:04:14Z
dc.date.available2017-06-29T06:04:14Z
dc.date.issued2008es_ES
dc.identifier607es_ES
dc.identifier.issn0270-6474es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/5291
dc.identifier.urihttps://doi.org/10.1523/JNEUROSCI.4848-08.2008es_ES
dc.language.isoenges_ES
dc.relation28 (52) 14042-14055 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnalysis of Variancees_ES
dc.subject.meshAnimalses_ES
dc.subject.meshAnimals, Newbornes_ES
dc.subject.meshBicuculline-pharmacologyes_ES
dc.subject.meshBiophysics-methodses_ES
dc.subject.meshCalcium-metabolismes_ES
dc.subject.meshCalcium Channel Blockers-pharmacologyes_ES
dc.subject.meshChelating Agents-pharmacologyes_ES
dc.subject.meshCyclopropanes-pharmacologyes_ES
dc.subject.meshEgtazic Acid-analogs & derivativeses_ES
dc.subject.meshEgtazic Acid-pharmacologyes_ES
dc.subject.meshElectric Stimulation-methodses_ES
dc.subject.meshExcitatory Amino Acid Antagonists-pharmacologyes_ES
dc.subject.meshGABA Antagonists-pharmacologyes_ES
dc.subject.meshGlycine-analogs & derivativeses_ES
dc.subject.meshGlycine-pharmacologyes_ES
dc.subject.meshHippocampus-cytologyes_ES
dc.subject.meshInterneurons-drug effectses_ES
dc.subject.meshInterneurons-physiologyes_ES
dc.subject.meshLong-Term Potentiation-drug effectses_ES
dc.subject.meshLong-Term Potentiation-physiologyes_ES
dc.subject.meshLysine-analogs & derivativeses_ES
dc.subject.meshLysine-metabolismes_ES
dc.subject.meshMalees_ES
dc.subject.meshMembrane Potentials-drug effectses_ES
dc.subject.meshMembrane Potentials-physiologyes_ES
dc.subject.meshMossy Fibers, Hippocampal-drug effectses_ES
dc.subject.meshMossy Fibers, Hippocampal-physiologyes_ES
dc.subject.meshNeuronal Plasticity-drug effectses_ES
dc.subject.meshNeuronal Plasticity-physiologyes_ES
dc.subject.meshNicotinic Antagonists-pharmacologyes_ES
dc.subject.meshNimodipine-pharmacologyes_ES
dc.subject.meshPatch-Clamp Techniques-methodses_ES
dc.subject.meshPolyamines-pharmacologyes_ES
dc.subject.meshRatses_ES
dc.subject.meshRats, Sprague-Dawleyes_ES
dc.subject.meshTime Factorses_ES
dc.titleBidirectional Hebbian plasticity at hippocampal mossy fiber synapses on CA3 interneuronses_ES
dc.typearticlees_ES
dc.contributor.affiliationDepartment of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.es_ES
dc.contributor.emailgerman@pitt.edues_ES
dc.relation.jnabreviadoJ NEUROSCIes_ES
dc.relation.journalThe Journal of Neurosciencees_ES
dc.identifier.placeUnited Stateses_ES
dc.date.published2008es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1529-2401es_ES
dc.identifier.doi10.1523/JNEUROSCI.4848-08.2008es_ES
dc.description.monthDices_ES
dc.description.abstractotrodiomaHippocampal area CA3 is critically involved in the formation of nonoverlapping neuronal subpopulations (‘pattern separation’) to store memory representations as distinct events. Efficient pattern separation relies on the strong and sparse excitatory input from the mossy fibers (MFs) to pyramidal cells and feedforward inhibitory interneurons. However, MF synapses on CA3 pyramidal cells undergo long-term potentiation (LTP), which, if unopposed, will degrade pattern separation because MF activation will now recruit additional CA3 pyramidal cells. Here, we demonstrate MF LTP in stratum lacunosum-moleculare (L-M) interneurons induced by the same stimulation protocol that induces MF LTP in pyramidal cells. This LTP was NMDA receptor (NMDAR) independent and occurred at MF Ca(2+)-impermeable AMPA receptor synapses. LTP was prevented by with voltage clamping the postsynaptic cell soma during high-frequency stimulation (HFS), intracellular injections of the Ca(2+) chelator BAPTA (20 mm), or bath applications of the L-type Ca(2+) channel blocker nimodipine (10 microm). We propose that MF LTP in L-M interneurons preserves the sparsity of pyramidal cell activation, thus allowing CA3 to maintain its role in pattern separation. In the presence of the mGluR1alpha antagonist LY367385 [(S)-(+)-a-amino-4-carboxy-2-methylbenzeneacetic acid] (100 microm), the same HFS that induces MF LTP in naive slices triggered NMDAR-independent MF LTD. This LTD, like LTP, required activation of the L-type Ca(2+) channel and also was induced after blockade of IP(3) receptors with heparin (4 mg-ml) or the selective depletion of receptor-gated Ca(2+) stores with ryanodine (10 or 100 microm). We conclude that L-M interneurons are endowed with Ca(2+) signaling cascades suitable for controlling the polarity of MF long-term plasticity induced by joint presynaptic and postsynaptic activities.es_ES
dc.subject.koMossy fiberes_ES
dc.subject.koLTPes_ES
dc.subject.koLTDes_ES
dc.subject.koCalcium-impermeable AMPARses_ES
dc.subject.koCA3 interneuronses_ES
dc.subject.koFeedforward inhibitiones_ES


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