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dc.contributor.authorAmpuero E.
dc.contributor.authorCerda M.
dc.contributor.authorHärtel S.
dc.contributor.authorRubio F.J.
dc.contributor.authorMassa S.
dc.contributor.authorCubillos P.
dc.contributor.authorAbarzúa-Catalán L.
dc.contributor.authorSandoval R.
dc.contributor.authorGalaburda A.M.
dc.contributor.authorWyneken U.
dc.date.accessioned2020-09-02T22:11:14Z
dc.date.available2020-09-02T22:11:14Z
dc.date.issued2019
dc.identifier10.3389/fphar.2019.00804
dc.identifier.citation10, , -
dc.identifier.issn16639812
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3564
dc.descriptionFluoxetine is a selective serotonin reuptake inhibitor (SSRI) used to treat mood and anxiety disorders. Chronic treatment with this antidepressant drug is thought to favor functional recovery by promoting structural and molecular changes in several forebrain areas. At the synaptic level, chronic fluoxetine induces an increased size and density of dendritic spines and an increased ratio of GluN2A over GluN2B N-methyl-D-aspartate (NMDA) receptor subunits. The “maturation”-promoting molecular changes observed after chronic fluoxetine should also induce structural remodeling of the neuronal dendritic arbor and changes in the synaptic responses. We treated adult rats with fluoxetine (0.7 mg/kg i.p. for 28 days) and performed a morphometric analysis using Golgi stain in limbic and nonlimbic cortical areas. Then, we focused especially on the auditory cortex, where we evaluated the dendritic morphology of pyramidal neurons using a 3-dimensional reconstruction of neurons expressing mRFP after in utero electroporation. With both methodologies, a shortening and decreased complexity of the dendritic arbors was observed, which is compatible with an increased GluN2A over GluN2B ratio. Recordings of extracellular excitatory postsynaptic potentials in the auditory cortex revealed an increased synaptic response after fluoxetine and were consistent with an enrichment of GluN2A-containing NMDA receptors. Our results confirm that fluoxetine favors maturation and refinement of extensive cortical networks, including the auditory cortex. The fluoxetine-induced receptor switch may decrease GluN2B-dependent toxicity and thus could be applied in the future to treat neurodegenerative brain disorders characterized by glutamate toxicity and/or by an aberrant network connectivity. © 2019 Ampuero, Cerda, Härtel, Rubio, Massa, Cubillos, Abarzúa-Catalán, Sandoval, Galaburda and Wyneken.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectAntidepressant
dc.subjectAuditory cortex
dc.subjectDendritic architecture
dc.subjectNeuronal segmentation
dc.subjectNMDA receptors
dc.subjectfluoxetine
dc.subjectmonomeric red fluorescent protein
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectn methyl dextro aspartic acid receptor 2A
dc.subjectn methyl dextro aspartic acid receptor 2B
dc.subjectred fluorescent protein
dc.subjectunclassified drug
dc.subjectadult
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectauditory cortex
dc.subjectbrain maturation
dc.subjectcontrolled study
dc.subjectdendritic spine
dc.subjectdrug effect
dc.subjectembryo
dc.subjectexcitatory postsynaptic potential
dc.subjectfemale
dc.subjectfetus
dc.subjectGolgi stain
dc.subjectlimbic cortex
dc.subjectmale
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectpyramidal nerve cell
dc.subjectrat
dc.subjectsynapse
dc.titleChronic fluoxetine treatment induces maturation-compatible changes in the dendritic arbor and in synaptic responses in the auditory cortex
dc.typeArticle


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