Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/58185

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dc.contributor.authorYu, S.por
dc.contributor.authorZutshi, I.por
dc.contributor.authorStoffel, R.por
dc.contributor.authorZhang, J.por
dc.contributor.authorVentura-Silva, A. P.por
dc.contributor.authorSousa, Nunopor
dc.contributor.authorCosta, P. S.por
dc.contributor.authorHolsboer, F.por
dc.contributor.authorPatchev, A.por
dc.contributor.authorAlmeida, O. F. X.por
dc.date.accessioned2019-01-14T23:49:50Z-
dc.date.available2019-01-14T23:49:50Z-
dc.date.issued2017-
dc.identifier.issn2158-3188-
dc.identifier.urihttp://hdl.handle.net/1822/58185-
dc.description.abstractThe dynamic turnover of hippocampal neurons is implicated in the regulation of cognitive and affective behavior. Extending our previous demonstration that administration of dexamethasone (ND) to neonatal rats depletes the resident population of neural precursor cells (NPC) and restrains the size of the neurogenic regions, we now show that the adverse effects of ND persist into adulthood. Specifically, ND impairs repletion of the neurogenic pool and neurogenesis; ND also compromises cognitive performance, the ability to actively adapt to an acute stressor and, the efficacy of glucocorticoid (GC) negative feedback. Interestingly, although ND depletes the neurogenic pool, it does not permanently abolish the proliferative machinery of the residual NPC population; however, ND increases the susceptibility of hippocampal granule neurons to apoptosis. Although the antidepressant fluoxetine (FLX) reverses the latter phenomenon, it does not replenish the NPC pool. Treatment of ND-treated adult rats with FLX also improves GC negative feedback, albeit without rescuing the deleterious effects of ND on behavior. In summary, ND leads to protracted disruption of mental functions, some of which are resistant to antidepressant interventions. We conclude that manipulation of the NPC pool during early life may jeopardize the therapeutic potential of antidepressants in adulthood.por
dc.description.sponsorshipWe thank Albin Varga and his team for invaluable help with animal housing and care. This study represents a contribution from the SwitchBox Consortium, supported by the European FP7 (Contract 259772), with additional suuport from the National Key Research & Development Program of China (2016YFC1306600) to YS. The funders did not have any role in the design or execution of the study and had no influence over the interpretation of its results or the writing of the paper. The research was conducted in the absence of commercial or financial relationships that could be construed as a potential conflict of interest.por
dc.language.isoengpor
dc.publisherNature Publishing Group (NPG)por
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/259772/EUpor
dc.rightsopenAccesspor
dc.subjectAnimalspor
dc.subjectAnimals, Newbornpor
dc.subjectAntidepressive Agentspor
dc.subjectApoptosispor
dc.subjectDexamethasonepor
dc.subjectFeedback, Physiologicalpor
dc.subjectFluoxetinepor
dc.subjectGlucocorticoidspor
dc.subjectHippocampuspor
dc.subjectMalepor
dc.subjectNeural Stem Cellspor
dc.subjectNeurogenesispor
dc.subjectNeuronspor
dc.subjectRatspor
dc.subjectRats, Wistarpor
dc.titleAntidepressant responsiveness in adulthood is permanently impaired after neonatal destruction of the neurogenic poolpor
dc.typearticlepor
dc.peerreviewedyespor
oaire.citationIssue1por
oaire.citationVolume7por
dc.identifier.doi10.1038/tp.2016.255por
dc.identifier.pmid28045461por
dc.description.publicationversioninfo:eu-repo/semantics/publishedVersionpor
dc.subject.wosScience & Technologypor
sdum.journalTranslational Psychiatrypor
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