A number of possible etiologies of atypical neural oscillations in ASD have been suggested, including: a surfeit in local connectivity – especially in primary sensory areas (Belmonte et al., 2004); smaller and more dispersed cortical mini-columns leading to a reduction in inhibitory inter-neuronal activity (Casanova et al., 2002); an imbalance of cortical excitation and inhibition due to increased glutamergic/reduced GABAergic signaling (Rubenstein and Merzenich, 2003); and impairment in the inferior olive – a structure that that mediates electrical synapses and that drives neural synchrony, and has been found to be structurally atypical in some individuals with ASD (Welsh et al., 2005). No theory has yet linked any of these putative impairments with increased intra-participant variability in those with ASD. However within the literature on ADHD, intra-participant variability has been theoretically linked with inconsistent and inefficient neuronal transmission, which may arise from impairment in astrocytes, a type of glial cell that plays a critical role in fueling neuronal oscillations (Russell et al., 2006). Astrocyte impairment in ASD could therefore account for a range of features of ASD including neural de-synchrony, EEG
