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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/56693
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dc.creatorLuiz Alexandre Viana Magnopt_BR
dc.creatorHelia Tenza Ferrerpt_BR
dc.creatorMélcar Collodettipt_BR
dc.creatorEduardo de Souza Nicolaupt_BR
dc.creatorJivan Khlghatyanpt_BR
dc.creatorThomas Del’Guidicept_BR
dc.creatorMarco Aurelio Romano Silvapt_BR
dc.creatorJean Martin Beaulieupt_BR
dc.date.accessioned2023-07-19T16:50:27Z-
dc.date.available2023-07-19T16:50:27Z-
dc.date.issued2020-
dc.citation.volume10pt_BR
dc.citation.issue4566pt_BR
dc.citation.spage1pt_BR
dc.citation.epage113pt_BR
dc.identifier.doihttps://doi.org/10.1038/s41598-020-61248-zpt_BR
dc.identifier.issn2045-2322pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/56693-
dc.description.resumoPeripheral biomarker and post-mortem brains studies have shown alterations of neuronal calcium sensor 1 (Ncs-1) expression in people with bipolar disorder or schizophrenia. However, its engagement by psychiatric medications and potential contribution to behavioral regulation remains elusive. We investigated the effect on Ncs-1 expression of valproic acid (VPA), a mood stabilizer used for the management of bipolar disorder. Treatment with VPA induced Ncs-1 gene expression in cell line while chronic administration of this drug to mice increased both Ncs-1 protein and mRNA levels in the mouse frontal cortex. Inhibition of histone deacetylases (HDACs), a known biochemical effect of VPA, did not alter the expression of Ncs-1. In contrast, pharmacological inhibition or genetic downregulation of glycogen synthase kinase 3β (Gsk3β) increased Ncs-1 expression, whereas overexpression of a constitutively active Gsk3β had the opposite effect. Moreover, adeno-associated virus-mediated Ncs-1 overexpression in mouse frontal cortex caused responses similar to those elicited by VPA or lithium in tests evaluating social and mood-related behaviors. These findings indicate that VPA increases frontal cortex Ncs-1 gene expression as a result of Gsk3 inhibition. Furthermore, behavioral changes induced by Ncs-1 overexpression support a contribution of this mechanism in the regulation of behavior by VPA and potentially other psychoactive medications inhibiting Gsk3 activity.pt_BR
dc.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentMED - DEPARTAMENTO DE SAÚDE MENTALpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofScientifc Reportspt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectNeuronal Calcium Sensor 1 (Ncs-1)pt_BR
dc.subjectBipolar disorderpt_BR
dc.subjectSchizophreniapt_BR
dc.subject.otherTranstorno bipolarpt_BR
dc.subject.otherEsquizofrenia paranoidept_BR
dc.subject.otherInibiçãopt_BR
dc.titleContribution of neuronal calcium sensor 1 (Ncs-1) to anxiolytic-like and social behavior mediated by valproate and Gsk3 inhibitionpt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.nature.com/articles/s41598-020-61248-zpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3693-1897pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9175-5761pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1236-6424pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7576-1101pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5628-8053pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4969-7016pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6558-4639pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0446-7447pt_BR
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