genetic deletion of the Dlgap3 gene in mice has been shown to result in a variety of OCD-like abnormalities such as extensive grooming, abnormal motor behavior, and anxiety (Welch et al., 2007). As a neurobiological consequence, loss of Dlgap3 expression has been reported to cause dorsal striatal impairments of glutamate receptor regulation and neurophysiological function (Wan et al., 2014; Wan et al., 2011). Dlg4/Psd-95 disturbances have also been linked with a variety of neuropsychiatric phenotypes such as schizophrenia, bipolar disorder and increased morphine sensitivity (de Bartolomeis et al., 2014; Dean et al., 2015; Hall et al., 2015; Kristiansen and Meador-Woodruff, 2005; Wang et al., 2014).
