Topic: Ts2Cje mouse model

In mouse models of Down syndrome (DS), cognitive deficits such as memory impairment are believed to be caused by overinhibition. However, recent studies indicate that the overexpression of Grik1, a gene mainly expressed at interneurons in the hippocampus, could be a key driver of memory deficits in individuals with DS due to a bidirectional alteration of synaptic inhibition on CA1 pyramidal cells (Valbuena et al, Nature Comms. 2019, 10:4991). Remarkably, normalizing Grik1 dosage in the Ts2Cje mouse model of DS specifically restores spatial memory and reverses the bidirectional alterations to C

Research has shown that individuals with Down syndrome experience altered pain sensitivity, with varying results depending on the type of nociceptive stimulus. GRIK1, a gene coding for the GluK1 subunit of kainate receptors is triplicated in Down syndrome. This subunit is heavily expressed in Dorsal Root Ganglion neurons and has been implicated in modulating pain perception. To investigate this further, we have conducted experiments in the Ts2Cje mouse model of Down syndrome, comparing them to mice lacking Grik1. The results suggest that altered pain perception in Down syndrome is dependent on