This observation was critical in motivating the assessment of L-LTP in Ts65Dn mice here, given that dysfunction of NMDA receptors in DS was originally theoretically predicted as the potential consequence of the inhibition of calcineurin activity due to overexpression of chromosome 21 gene products such as RCAN1 and DYRK1A (perhaps coupled to elevated amounts of reactive oxidative species) [42]. This evidence concerns the gene RCAN1 and Dravet syndrome.