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Cerebral Cortex, Vol. 13, No. 7, 758-764, July 2003
© 2003 Oxford University Press

Alterations of Neocortical Pyramidal Cell Phenotype in the Ts65Dn Mouse Model of Down Syndrome: Effects of Environmental Enrichment

M. Dierssen, R. Benavides-Piccione1, C. Martínez-Cué2, X. Estivill, J. Flórez2, G.N. Elston1,3 and J. DeFelipe1

Program in Genes and Disease, Genomic Regulation Center, 08003 Barcelona, , 1 Cajal Institute, 28002 Madrid, , 2 Department of Physiology and Pharmacology, University of Cantabria, 39011 Santander, Spain and , 3 Vision, Touch & Hearing Research Centre, Department of Physiology & Pharmacology, School of Biomedical Sciences, The University of Queensland, Australia

Mental retardation in individuals with Down syndrome (DS) is thought to result from anomalous development and function of the brain; however, the underlying neuropathological processes have yet to be determined. Early implementation of special care programs result in limited, and temporary, cognitive improvements in DS individuals. In the present study, we investigated the possible neural correlates of these limited improvements. More specifically, we studied cortical pyramidal cells in the frontal cortex of Ts65Dn mice, a partial trisomy of murine chromosome 16 (MMU16) model characterized by cognitive deficits, hyperactivity, behavioral disruption and reduced attention levels similar to those observed in DS, and their control littermates. Animals were raised either in a standard or in an enriched environment. Environmental enrichment had a marked effect on pyramidal cell structure in control animals. Pyramidal cells in environmentally enriched control animals were significantly more branched and more spinous than non-enriched controls. However, environmental enrichment had little effect on pyramidal cell structure in Ts65Dn mice. As each dendritic spine receives at least one excitatory input, differences in the number of spines found in the dendritic arbors of pyramidal cells in the two groups reflect differences in the number of excitatory inputs they receive and, consequently, complexity in cortical circuitry. The present results suggest that behavioral deficits demonstrated in the Ts65Dn model could be attributed to abnormal circuit development.


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