Down syndrome (DS) is the most common genetic disease underlying intellectual disability. It is characterized by memory impairment and brain morphological and molecular alterations resulting in poor executive performance. Different mouse models have been developed to understand DS, Ts65Dn being the best characterized. Even though a lot is known about genetic, morphological and molecular abnormalities in this model, neural activity alterations are poorly understood. It has been described that environmental ...
Down syndrome (DS) is the most common genetic disease underlying intellectual disability. It is characterized by memory impairment and brain morphological and molecular alterations resulting in poor executive performance. Different mouse models have been developed to understand DS, Ts65Dn being the best characterized. Even though a lot is known about genetic, morphological and molecular abnormalities in this model, neural activity alterations are poorly understood. It has been described that environmental enrichment (EE) and the green tea extract epigallocatequine-3-gallate (EGCG) rescue cognitive impairment in Ts65Dn mice; however, the cellular mechanisms underlying their therapeutic action are not well understood. The present work reports the presence of an aberrant prefrontal cortex and hippocampal multi-unit activity (MUA) in Ts65Dn mice when compared to wild-type non-trisomic mice. The results show that EE and EGCG, when administered in combination, normalize this aberrant neural activity of trisomic mice, although, statistically significant differences were only reported in the prefrontal cortex. Therefore, additional data needs to be analysed to enhance statistical robustness and demonstrate further this effect also in the hippocampus. Aside its limitations, this work provides novel and valuable neurophysiological information that may be used to understand DS cognitive normalization both in mouse models and humans.
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