Publication: Morphological alterations in the hippocampus of the Ts65Dn mouse model for Down syndrome correlate with structural plasticity markers
Authors
Villarroya, Olga ; Ballestín, Raúl ; López Hidalgo, Rosa ; Mulet, Maria ; Blasco Ibáñez, José Miguel ; Crespo, Carlos ; Nacher, Juan ; Gilabert Juan, Javier ; Varea, Emilio
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-11-894
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info:eu-repo/semantics/article
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.
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Citation
Histology and Histopathology, Vol.33, nº1, (2018)
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