There are some glaring missing links in our understanding of the pathophysiology of ASDs. Specifically, how the mutation of an individual gene, a disrupted molecular pathway, and dysfunctional synapses affect the circuitry and produce ASD-like behavioral manifestations is unclear. Understanding the circuitry underlying autism, both anatomically and functionally, is critical to the development of effective clinical intervention. Several competing hypotheses regarding the circuit-level mechanisms have been proposed in the human literature. One widely tested hypothesis is altered structural and functional brain connectivity (Belmonte et al., 2004; Geschwind and Levitt, 2007; Kana et al., 2014). Structural connectivity is the physical connections between different brain regions, while functional connectivity refers to the integrated relationship between spatially separated brain regions. It is believed that structural connections within the brain give rise to functional network activity as measured by coherence or information flow. Neuroimaging 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
