mGluR5-dependent modulation of dendritic excitability in CA1 pyramidal neurons mediated by enhancement of persistent Na+ currents

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dc.contributor.authorYu, Weonjinko
dc.contributor.authorKwon, Jaehanko
dc.contributor.authorSohn, Jong-Wooko
dc.contributor.authorLee, Suk Hoko
dc.contributor.authorKim, Sooyunko
dc.contributor.authorHo, Won-Kyungko
dc.date.accessioned2018-10-19T00:30:58Z-
dc.date.available2018-10-19T00:30:58Z-
dc.date.created2018-09-19-
dc.date.created2018-09-19-
dc.date.issued2018-09-
dc.identifier.citationJOURNAL OF PHYSIOLOGY-LONDON, v.596, no.17, pp.4141 - 4156-
dc.identifier.issn0022-3751-
dc.identifier.urihttp://hdl.handle.net/10203/245907-
dc.description.abstractDendritic Na+ channels in pyramidal neurons are known to amplify synaptic signals, thereby facilitating action potential (AP) generation. However, the mechanisms that modulate dendritic Na+ channels have remained largely uncharacterized. Here, we report a new form of short-term plasticity in which proximal excitatory synaptic inputs to hippocampal CA1 pyramidal neurons transiently elevate dendritic excitability. High-frequency stimulations (HFS) to the Schaffer collateral (SC) pathway activate mGluR5-dependent Ca2+ signalling in the apical dendrites, which, with calmodulin, upregulates specifically Nav1.6 channel-mediated persistent Na+ currents (I-Na,I-P) in the dendrites. This HFS-induced increase in dendritic I-Na,I-P results in transient increases in the amplitude of excitatory postsynaptic potentials induced by both proximal SC and distal perforant path stimulation, leading to the enhanced probability of AP firing associated with decreased AP thresholds. Taken together, our study identifies dendritic I-Na,I-P as a novel target for mediating activity-dependent modulation of dendritic integration and neuronal output.-
dc.languageEnglish-
dc.publisherWILEY-
dc.subjectMETABOTROPIC GLUTAMATE RECEPTORS-
dc.subjectBACKPROPAGATING ACTION-POTENTIALS-
dc.subjectLONG-TERM POTENTIATION-
dc.subjectSODIUM-CHANNELS-
dc.subjectSYNAPTIC INTEGRATION-
dc.subjectHIPPOCAMPAL-NEURONS-
dc.subjectSENSORY NEURONS-
dc.subjectI-H-
dc.subjectACTIVATION-
dc.subjectPLASTICITY-
dc.titlemGluR5-dependent modulation of dendritic excitability in CA1 pyramidal neurons mediated by enhancement of persistent Na+ currents-
dc.typeArticle-
dc.identifier.wosid000443233300031-
dc.identifier.scopusid2-s2.0-85052512454-
dc.type.rimsART-
dc.citation.volume596-
dc.citation.issue17-
dc.citation.beginningpage4141-
dc.citation.endingpage4156-
dc.citation.publicationnameJOURNAL OF PHYSIOLOGY-LONDON-
dc.identifier.doi10.1113/JP275999-
dc.contributor.localauthorSohn, Jong-Woo-
dc.contributor.nonIdAuthorYu, Weonjin-
dc.contributor.nonIdAuthorKwon, Jaehan-
dc.contributor.nonIdAuthorLee, Suk Ho-
dc.contributor.nonIdAuthorKim, Sooyun-
dc.contributor.nonIdAuthorHo, Won-Kyung-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordAuthormGluR5 signaling-
dc.subject.keywordAuthordendritic excitability-
dc.subject.keywordAuthorpersistent sodium current-
dc.subject.keywordPlusMETABOTROPIC GLUTAMATE RECEPTORS-
dc.subject.keywordPlusBACKPROPAGATING ACTION-POTENTIALS-
dc.subject.keywordPlusLONG-TERM POTENTIATION-
dc.subject.keywordPlusSODIUM-CHANNELS-
dc.subject.keywordPlusSYNAPTIC INTEGRATION-
dc.subject.keywordPlusHIPPOCAMPAL-NEURONS-
dc.subject.keywordPlusSENSORY NEURONS-
dc.subject.keywordPlusI-H-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusPLASTICITY-
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