A sustained reduction in LTP was previously reported in a conditional DM1 mouse model expressing high levels of interrupted CUG RNA repeats in the brain [50], and in Mbnl2 knockouts, in association with altered NMDAR activity and modest mis-splicing of exon 5 of Grin1 (glutamate ionotropic receptor NMDA-type subunit, also named Nmdar1) [26], which regulates receptor potentiation [51]. The gene discussed is GRIN1; the disease is myotonic dystrophy type 1.