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Despite extensive research, the causes of Autistic Spectrum Disorders (ASD) are still unknown and no single explanation has been proposed that can account for the heterogeneous profile (Muller, 2007). The DSM-IV diagnostic criteria for ASD include deficits in social and communicative skills such as imitation, empathy, and shared attention, as well as restricted interests and repetitive patterns of behaviors. Elucidating the neuroetiology of these symptoms has been a challenge because the behavioral manifestations vary both in severity (high, medium, or low) as well as expression (Autistic Disorder, Asperger Syndrome, or Pervasive Developmental Disorder-Not Otherwise Specified) (Matson, 2006; Volkmar et al., 1994). Although a growing body of work has raised questions about the role of mirror neurons in human social behavior (Hickok, 2009; Lingnau et al., 2009), many recent studies suggest that a dysfunction in the frontal human mirror neuron system (hMNS) could potentially account for the social deficits in autism, including problems with imitation, understanding actions, emotion recognition, and empathy (Williams et al., 2001; Oberman et al., 2005; Dapretto et al., 2006; Williams et al., 2006). Mirror neurons were initially reported by Rizzolatti and colleagues (di Pellegrino et al., 1992) in the premotor cortex of macaque monkeys (area F5), an area thought to be analogous to Broca’s area (Brodmann’s area 44) in humans (Buccino et al., 2001; Buccino et al., 2004; Petrides et al., 2005). Some cells in this region increase firing during the execution of an action as well as during observation of a similar action performed by others. This execution/observation matching feature is hypothesized to provide a mechanism for

Behavioral and Electrophysiological Characterization of Induced Neural Plasticity in the Autistic Brain