Similarly—and in notable contrast to the findings from most other mouse models based upon schizophrenia risk genes—the preponderance of manipulations of NRG1 signaling have not revealed alterations in short-term glutamatergic synaptic plasticity suggesting NRG1 signaling may preferentially act postsynaptically at these synapses (Huang et al., 2000; Kwon et al., 2005; Iyengar and Mott, 2008; Pitcher et al., 2008; Chen et al., 2010; but see Bjarnadottir et al., 2007; Woo et al., 2007; Deakin et al., 2012). Here, NRG1 is linked to schizophrenia.