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Hypocellularity in the Murine Model for Down Syndrome Ts65Dn Is Not Affected by Adult Neurogenesis.

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Hypocellularity in the Murine Model for Down Syndrome Ts65Dn Is Not Affected by Adult Neurogenesis.

dc.contributor.author	López Hidalgo, Rosa
dc.contributor.author	Ballestín Hinojosa, Raúl
dc.contributor.author	Vega,Jessica
dc.contributor.author	Blasco Ibáñez, José Miguel
dc.contributor.author	Crespo Rupérez, Carlos
dc.contributor.author	Gilabert Juan, Javier
dc.contributor.author	Nácher Roselló, Juan Salvador
dc.contributor.author	Varea López, Emilio
dc.date.accessioned	2020-05-08T18:32:03Z
dc.date.available	2020-05-08T18:32:03Z
dc.date.issued	2016
dc.identifier.citation	López Hidalgo, Rosa Ballestín Hinojosa, Raúl Vega,Jessica Blasco Ibáñez, José Miguel Crespo Rupérez, Carlos Gilabert Juan, Javier Nácher Roselló, Juan Salvador Varea López, Emilio 2016 Hypocellularity in the Murine Model for Down Syndrome Ts65Dn Is Not Affected by Adult Neurogenesis. Frontiers In Neuroscience
dc.identifier.uri	https://hdl.handle.net/10550/74548
dc.description.abstract	Down syndrome (DS) is caused by the presence of an extra copy of the chromosome 21 and it is the most common aneuploidy producing intellectual disability. Neural mechanisms underlying this alteration may include defects in the formation of neuronal networks, information processing and brain plasticity. The murine model for DS, Ts65Dn, presents reduced adult neurogenesis. This reduction has been suggested to underlie the hypocellularity of the hippocampus as well as the deficit in olfactory learning in the Ts65Dn mice. Similar alterations have also been observed in individuals with DS. To determine whether the impairment in adult neurogenesis is, in fact, responsible for the hypocellularity in the hippocampus and physiology of the olfactory bulb, we have analyzed cell proliferation and neuronal maturation in the two major adult neurogenic niches in the Ts656Dn mice: the subgranular zone (SGZ) of the hippocampus and the subventricular zone (SVZ). Additionally, we carried out a study to determine the survival rate and phenotypic fate of newly generated cells in both regions, injecting 5′BrdU and sacrificing the mice 21 days later, and analyzing the number and phenotype of the remaining 5′BrdU-positive cells. We observed a reduction in the number of proliferating (Ki67 positive) cells and immature (doublecortin positive) neurons in the subgranular and SVZ of Ts65Dn mice, but we did not observe changes in the number of surviving cells or in their phenotype. These data correlated with a lower number of apoptotic cells (cleaved caspase 3 positive) in Ts65Dn. We conclude that although adult Ts65Dn mice have a lower number of proliferating cells, it is compensated by a lower level of cell death. This higher survival rate in Ts65Dn produces a final number of mature cells similar to controls. Therefore, the reduction of adult neurogenesis cannot be held responsible for the neuronal hypocellularity in the hippocampus or for the olfactory learning deficit of Ts65Dn mice
dc.language.iso	eng
dc.relation.ispartof	Frontiers In Neuroscience, 2016
dc.subject	Psicobiologia
dc.subject	Biotecnologia
dc.title	Hypocellularity in the Murine Model for Down Syndrome Ts65Dn Is Not Affected by Adult Neurogenesis.
dc.type	journal article	es_ES
dc.date.updated	2020-05-08T18:32:04Z
dc.identifier.doi	10.3389/fnins.2016.00075
dc.identifier.idgrec	115599
dc.rights.accessRights	open access	es_ES