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 single-trial variability, and behavioral (response time) variability. Given the important role of glia in synapse formation and maintenance (Bolton and Eroglu, 2009) the suggestion that astrocyte impairment may be a critical factor in ASD is a tantalizing one. It is important to note however that, in addition to the theoretically formulated suggestions described above, a variety of neuronal characteristics (e.g., synaptic transmission, channel gating, fluctuation in transmitter release, postsynaptic receptor activation, ion concentrations, membrane conductance) may contribute to variability of evoked EEG response (Sannita, 2006), therefore it is not currently possible to identify the precise source(s) of EEG variability.
