René’s co-first author publication, titled “DSCAM gene triplication causes excessive GABAergic synapses in the neocortex in Down syndrome mouse models” was accepted for publication in PLOS Biology. This was a collaborative effort between our group and the Bing Ye lab in the Life Science Institute at the University of Michigan. Down syndrome is caused by the trisomy of human chromosome 21 (HSA21). The Down syndrome cell adhesion molecule (DSCAM) gene is located on HSA21. In this study, we investigated the role of DSCAM in regulating GABAergic synapses formed on neocortical pyramidal neurons in the Ts65Dn mouse model for Down syndrome, where DSCAM is overexpressed. We found that excessive GABAergic innervations of cortical Pyramidal neurons (PyNs) by basket and chandelier cells are increased in this model. However, genetic normalization of DSCAM expression rescues this excessive innervation and inhibition of PyNs. Conversely, loss of DSCAM impairs GABAergic synapse development and function. These findings demonstrate that DSCAM overexpression causes excessive GABAergic innervation and synaptic transmission in the neocortex of Down syndrome mouse models. They also suggest that dysregulated DSCAM levels could be a pathogenic driver in related neurological disorders. Congrats, René and team! Read more here.