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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/164690
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dc.contributor.authorIbi, Daisuke-
dc.contributor.authorLópez-Giménez, Juan F.-
dc.contributor.authorMeana, J. J.-
dc.contributor.authorGonzález-Maeso, Javier-
dc.date.accessioned2018-05-10T11:59:58Z-
dc.date.available2018-05-10T11:59:58Z-
dc.date.issued2017-
dc.identifierdoi: 10.1038/nn.4616-
dc.identifiere-issn: 1546-1726-
dc.identifierissn: 1097-6256-
dc.identifier.citationNature Neuroscience 20(9): 1247-1259 (2017)-
dc.identifier.urihttp://hdl.handle.net/10261/164690-
dc.descriptionIbi, Daisuke et al.-
dc.description.abstractAntipsychotic drugs remain the standard for schizophrenia treatment. Despite their effectiveness in treating hallucinations and delusions, prolonged exposure to antipsychotic medications leads to cognitive deficits in both schizophrenia patients and animal models. The molecular mechanisms underlying these negative effects on cognition remain to be elucidated. Here we demonstrate that chronic antipsychotic drug exposure increases nuclear translocation of NF-κB in both mouse and human frontal cortex, a trafficking event triggered via 5-HT-receptor-dependent downregulation of the NF-κB repressor IκBα. This upregulation of NF-κB activity led to its increased binding at the Hdac2 promoter, thereby augmenting Hdac2 transcription. Deletion of HDAC2 in forebrain pyramidal neurons prevented the negative effects of antipsychotic treatment on synaptic remodeling and cognition. Conversely, virally mediated activation of NF-κB signaling decreased cortical synaptic plasticity via HDAC2. Together, these observations may aid in developing therapeutic strategies to improve the outcome of schizophrenia treatment.-
dc.description.sponsorshipNIH R01 MH084894 (J.G.M.), NIH R01 MH111940 (J.G.M.), Dainippon Sumitomo Pharma (J.G.M.), NARSAD (J.G.M.), the Japan Society for the Promotion of Science (JSPS) 15H06719 and 16K19786 (D.I.), NIH R01 MH104491 (G.W.H.), NIH R01 MH086509 (S.A.), NIH P50 MH096890 (S.A.), MINECO/ERDF SAF2009-08460 (J.J.M. and L.F.C.), SAF2013-45084R (J.J.M. and L.F.C.), Basque Government IT616-13 (J.J.M.), NIH R21 MH103877 (S.D.) and NIH R01 MH090264 (S.J.R.) participated in the funding of this study. RNA-seq analysis was supported in part through the computational resources and staff expertise provided by Scientific Computing at the Icahn School of Medicine at Mount Sinai and the NIH infrastructure grant S10OD018522. C.M. and A.G.B. were recipients of a postdoctoral and a predoctoral fellowship from the Basque Government, respectively. D.I. was a recipient of postdoctoral fellowships from JSPS (Young Scientists JSPS 23-3454) and the Uehara Memorial Foundation.-
dc.publisherNature Publishing Group-
dc.relationinfo:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2013-45084-R-
dc.relation.isversionofPostprint-
dc.rightsopenAccess-
dc.titleAntipsychotic-induced Hdac2 transcription via N-FκB leads to synaptic and cognitive side effects-
dc.typeartículo-
dc.identifier.doi10.1038/nn.4616-
dc.relation.publisherversionhttps://doi.org/10.1038/nn.4616-
dc.date.updated2018-05-10T11:59:58Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderJapan Society for the Promotion of Science-
dc.contributor.funderNational Institutes of Health (US)-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderEuropean Commission-
dc.contributor.funderEusko Jaurlaritza-
dc.contributor.funderUehara Memorial Foundation for International Students-
dc.contributor.funderIcahn School of Medicine at Mount Sinai-
dc.relation.csicSí-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100001691es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100000002es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100007277es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003086es_ES
dc.identifier.pmid28783139-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.grantfulltextopen-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
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