Contribution of neuronal calcium sensor 1 (Ncs-1) to anxiolytic-like and social behavior mediated by valproate and Gsk3 inhibition

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dc.creatorLuiz Alexandre Viana Magno
dc.creatorHelia Tenza Ferrer
dc.creatorMélcar Collodetti
dc.creatorEduardo de Souza Nicolau
dc.creatorJivan Khlghatyan
dc.creatorThomas Del’Guidice
dc.creatorMarco Aurelio Romano Silva
dc.creatorJean Martin Beaulieu
dc.date.accessioned2023-07-19T16:50:27Z
dc.date.accessioned2025-09-08T23:05:20Z
dc.date.available2023-07-19T16:50:27Z
dc.date.issued2020
dc.identifier.doihttps://doi.org/10.1038/s41598-020-61248-z
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/1843/56693
dc.languagepor
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofScientifc Reports
dc.rightsAcesso Aberto
dc.subjectTranstorno bipolar
dc.subjectEsquizofrenia paranoide
dc.subjectInibição
dc.subject.otherNeuronal Calcium Sensor 1 (Ncs-1)
dc.subject.otherBipolar disorder
dc.subject.otherSchizophrenia
dc.titleContribution of neuronal calcium sensor 1 (Ncs-1) to anxiolytic-like and social behavior mediated by valproate and Gsk3 inhibition
dc.typeArtigo de periódico
local.citation.epage113
local.citation.issue4566
local.citation.spage1
local.citation.volume10
local.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.
local.identifier.orcidhttps://orcid.org/0000-0003-3693-1897
local.identifier.orcidhttps://orcid.org/0000-0002-9175-5761
local.identifier.orcidhttps://orcid.org/0000-0003-1236-6424
local.identifier.orcidhttps://orcid.org/0000-0001-7576-1101
local.identifier.orcidhttps://orcid.org/0000-0002-5628-8053
local.identifier.orcidhttps://orcid.org/0000-0003-4969-7016
local.identifier.orcidhttps://orcid.org/0000-0002-6558-4639
local.identifier.orcidhttps://orcid.org/0000-0002-0446-7447
local.publisher.countryBrasil
local.publisher.departmentMED - DEPARTAMENTO DE SAÚDE MENTAL
local.publisher.initialsUFMG
local.url.externahttps://www.nature.com/articles/s41598-020-61248-z

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