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

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dc.contributor.author Villarroya, Olga
dc.contributor.author Ballestín Hinojosa, Raúl
dc.contributor.author López Hidalgo, Rosa
dc.contributor.author Mulet, María
dc.contributor.author Blasco Ibáñez, José Miguel
dc.contributor.author Crespo, C.
dc.contributor.author Nácher Roselló, Juan Salvador
dc.contributor.author Gilabert Juan, Javier
dc.contributor.author Varea López, Emilio
dc.date.accessioned 2020-04-28T15:35:59Z
dc.date.available 2020-04-28T15:35:59Z
dc.date.issued 2018
dc.identifier.uri https://hdl.handle.net/10550/74105
dc.description.abstract Down 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.
dc.language.iso eng
dc.relation.ispartof Histology and Histopathology, 2018, vol. 33, num. 1, p. 101-115
dc.rights.uri info:eu-repo/semantics/openAccess
dc.source Villarroya, Olga Ballestín Hinojosa, Raúl López Hidalgo, Rosa Mulet, María Blasco Ibánez, José Miguel Crespo, C. Nácher Roselló, Juan Salvador Gilabert Juan, Javier Varea López, Emilio 2018 Morphological alterations in the hippocampus of the Ts65Dn mouse model for Down Syndrome correlate with structural plasticity markers Histology and Histopathology 33 1 101 115
dc.subject Psicobiologia
dc.subject Biotecnologia
dc.subject Patologia
dc.title Morphological alterations in the hippocampus of the Ts65Dn mouse model for Down Syndrome correlate with structural plasticity markers
dc.type info:eu-repo/semantics/article
dc.date.updated 2020-04-28T15:35:59Z
dc.identifier.doi https://doi.org/10.14670/HH-11-894
dc.identifier.idgrec 122499

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