Show simple item record

dc.contributor.authorSouza, Daniela Fraga dept_BR
dc.contributor.authorWartchow, Krista Minéiapt_BR
dc.contributor.authorLunardi, Paula Santanapt_BR
dc.contributor.authorBrolese, Giovanapt_BR
dc.contributor.authorTortorelli, Lucas Silvapt_BR
dc.contributor.authorBatassini, Cristianept_BR
dc.contributor.authorBiasibetti, Reginapt_BR
dc.contributor.authorGoncalves, Carlos Alberto Saraivapt_BR
dc.date.accessioned2018-04-26T02:32:44Zpt_BR
dc.date.issued2015pt_BR
dc.identifier.issn1662-5102pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/175021pt_BR
dc.description.abstractData from epidemiological studies suggest that prenatal exposure to bacterial and viral infection is an important environmental risk factor for schizophrenia. The maternal immune activation (MIA) animal model is used to study how an insult directed at the maternal host can have adverse effects on the fetus, leading to behavioral and neurochemical changes later in life. We evaluated whether the administration of LPS to rat dams during late pregnancy affects astroglial markers (S100B and GFAP) of the offspring in later life. The frontal cortex and hippocampus were compared in male and female offspring on postnatal days (PND) 30 and 60. The S100B protein exhibited an age-dependent pattern of expression, being increased in the frontal cortex and hippocampus of the MIA group at PND 60, while at PND 30, male rats presented increased S100B levels only in the frontal cortex. Considering that S100B secretion is reduced by elevation of glutamate levels, we may hypothesize that this early increment in frontal cortex tissue of males is associated with elevated extracellular levels of glutamate and glutamatergic hypofunction, an alteration commonly associated with SCZ pathology. Moreover, we also found augmented GFAP in the frontal cortex of the LPS group at PND 30, but not in the hippocampus. Taken together data indicate that astroglial changes induced by MIA are dependent on sex and brain region and that these changes could reflect astroglial dysfunction. Such alterations may contribute to our understanding of the abnormal neuronal connectivity and developmental aspects of SCZ and other psychiatric disorders.en
dc.format.mimetypeapplication/pdf
dc.language.isoengpt_BR
dc.relation.ispartofFrontiers in cellular neuroscience. Lausanne. Vol. 9 (Dec. 2015), 489, [11 p.]pt_BR
dc.rightsOpen Accessen
dc.subjectAnimal modelen
dc.subjectEsquizofreniapt_BR
dc.subjectAstrogliosisen
dc.subjectImunidade materno-adquiridapt_BR
dc.subjectGFAPen
dc.subjectSubunidade beta da proteína ligante de cálcio S100pt_BR
dc.subjectModelos animaispt_BR
dc.subjectLipopolysaccharideen
dc.subjectRatos Wistarpt_BR
dc.subjectSchizophreniaen
dc.subjectS100Ben
dc.titleChanges in astroglial markers in a maternal immune activation model of schizophrenia in wistar rats are dependent on sexpt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001065713pt_BR
dc.type.originEstrangeiropt_BR


Files in this item

Thumbnail
   

This item is licensed under a Creative Commons License

Show simple item record