We conclude that increased expression of Kcnj6 necessarily contributes to abnormal synaptic plasticity in the Ts65Ds mouse, raising the possibility that excessive signaling through Kir3.2 channels is implicated. Studies of the biology of Kir3.2 subunit-containing potassium channels and development of novel approaches to reduce the effect of increased Kir3.2 expression may offer a means to moderate cognitive deficits in DS.
