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Morphological alterations in the hippocampus of the Ts65Dn mouse model for Down syndrome correlate with structural plasticity markers

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dc.contributor.authorVillarroya, Olga
dc.contributor.authorBallestín, Raúl
dc.contributor.authorLópez Hidalgo, Rosa
dc.contributor.authorMulet, Maria
dc.contributor.authorBlasco Ibáñez, José Miguel
dc.contributor.authorCrespo, Carlos
dc.contributor.authorNacher, Juan
dc.contributor.authorGilabert Juan, Javier
dc.contributor.authorVarea, Emilio
dc.date.accessioned2022-03-24T12:07:00Z
dc.date.available2022-03-24T12:07:00Z
dc.date.issued2018
dc.description.abstractDown syndrome (DS) is the most common chromosomal aneuploidy. Although trisomy on chromosome 21 can display variable phenotypes, there is a common feature among all DS individuals: the presence of intellectual disability. This condition is partially attributed to abnormalities found in the hippocampus of individuals with DS and in the murine model for DS, Ts65Dn. To check if all hippocampal areas were equally affected in 4-5 month adult Ts65Dn mice, we analysed the morphology of dentate gyrus granule cells and cornu ammonis pyramidal neurons using Sholl method on Golgi-Cox impregnated neurons. Structural plasticity has been analysed using immunohistochemistry for plasticity molecules followed by densitometric analysis (Brain Derived Neurotrophic Factor (BDNF), Polysialylated form of the Neural Cell Adhesion Molecule (PSA-NCAM) and the Growth Associated Protein 43 (GAP43)). We observed an impairment in the dendritic arborisation of granule cells, but not in the pyramidal neurons in the Ts65Dn mice. When we analysed the expression of molecules related to structural plasticity in trisomic mouse hippocampus, we observed a reduction in the expression of BDNF and PSA-NCAM, and an increment in the expression of GAP43. These alterations were restricted to the regions related to dentate granule cells suggesting an interrelation. Therefore the impairment in dendritic arborisation and molecular plasticity is not a general feature of all Down syndrome principal neurons. Pharmacological manipulations of the levels of plasticity molecules could provide a way to restore granule cell morphology and function.es
dc.formatapplication/pdfes
dc.format.extent15es
dc.identifier.citationHistology and Histopathology, Vol.33, nº1, (2018)
dc.identifier.doiDOI: 10.14670/HH-11-894
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/118286
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectPSA-NCAMes
dc.subjectBDNFes
dc.subjectGranule cellses
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleMorphological alterations in the hippocampus of the Ts65Dn mouse model for Down syndrome correlate with structural plasticity markerses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.33, nº1 (2018)