investigations indicate that ASDs are associated with perturbed connectivity at both structural and functional levels (Minshew and Keller, 2010; Vissers et al., 2012); however, the exact nature and pattern of this aberrant neural connectivity remains uncertain due to inconsistent findings from neuroimaging studies in patients (Di Martino et al., 2014; Kana et al., 2014; Uddin et al., 2013). While early studies reported reduced functional connectivity (Just et al., 2004), recent investigations implicate hyper-connectivity in multiple brain regions and across neural circuits (Keown et al., 2013; Supekar et al., 2013). In addition to methodological and conceptual controversy, this uncertainty reflects the substantial molecular heterogeneity of human patients. Notably, these studies were conducted primarily in high-functioning ASD patients for whom the etiologies are mostly unknown. For these reasons, autism animal models offer a unique opportunity to test the functional connectivity hypothesis because of homogenous genetic defects. Using optogenetic tools, Gunaydin et al. have shown that the activity of ventral tegmental area (VTA) to nucleus accumbens (NAc) projections could encode and predict key features of social interaction in wild type mice (Gunaydin et al., 2014). Similarly, Felix-Ortix and Tye revealed the role of projections from the basolateral complex of the amygdala (BLA) to
