GRIN2B and juvenile Huntington disease: For example, NMDAR hypofunction has been reported in mouse models of schizophrenia (Mohn et al., 1999), increased GluN2B surface expression is observed in Huntington’s disease (Fan and Raymond, 2007; Milnerwood et al., 2010) and genetic evidence clearly implicates association of autism with the NMDA receptor subunit GluN2B (Tarabeux et al., 2011; Yoo et al., 2012).