A number of mRNA expression abnormalities seem to develop later in life (by early adulthood) in the dorsal striatum of both male and female offspring. This is interesting given that a number of neuropsychiatric disorders, including obsessive-compulsive disorder (OCD), also show a developmental progression and symptoms appear gradually over time, with clinical penetrance often evident in adulthood (Casey et al., 2015; Lenze and Wetherell, 2011; Schmitt et al., 2014). Indeed, a number of the genes currently investigated are relevant to some of these disorders. For example, genetic polymorphisms in the Dlgap3 gene, which encodes the Sapap3 protein that is a component of the postsynaptic density and interacts with Psd-95 physically and functionally, have been associated with a higher incidence of phenotypes within the OCD spectrum in humans (Bienvenu et al., 2009; Crane et al., 2011; Wu et al., 2013). Similarly, 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
