Mirror neurons - neurons that fire when a monkey performs an action as well as when it observes others perform the same action - provide a plausible neurophysiological mechanism for understanding not only the actions of others but also their intentions and emotions. Accordingly, mirror neurons can impact a variety of important social skills and behaviors that are aberrant in autism spectrum disorders (ASD), including imitation, empathy, and theory of mind. Indeed, using different methods and imaging techniques, several recent investigations have provided converging evidence linking a dysfunctional mirror neuron system (MNS) to core deficits in ASD.
In a previous fMRI study, we found that high-functioning children with ASD showed no significant MNS activity during observation and imitation of emotional expressions, and that the level of MNS activity observed within this group was strongly and inversely correlated with symptom severity in the social domain. In two other recent fMRI studies, we have shown that ASD children (i) could recruit normative neural networks when interpreting a speaker's communicative intent if explicit instructions are provided to direct their attention to the speaker's facial expression, but (ii) failed to activate the basal ganglia during an implicit language learning task. Building on these earlier findings, the first aim of the proposed project is to examine whether the MNS can be brought 'online' in children with ASD by manipulating their attention via task instructions, in order to begin to address whether MNS dysfunction is likely to be a cause or an effect of the lack of attentional preference for the human face that characterizes this disorder. Our second aim is to examine the functioning of the MNS in children with ASD who previously participated in a randomized controlled intervention study (headed by our collaborator, Dr. Kasari), in order to relate MNS activity to type of treatment received (joint attention vs. social play vs. control), as well to post-treatment gains on behavioral measures of interest (e.g., joint attention, imitation, language).
Our third aim is to investigate the reward system in ASD - a system known to modulate implicit learning in both animal and human models - as well as to explore the interface between reward and mirror neuron circuitry since the frontal component of the MNS is connected (via the insula) not only to limbic structures involved in emotion processing (e.g., the amygdala) but also with the ventral striatum, a basal ganglia region critically implicated in reward processing. Taken together, deficits in mirror neuron and striatal function can provide a unifying account for all core symptoms observed in ASD. Thus, research findings from the proposed studies should provide a better characterization of the neural underpinnings of autism which, in turn, should lead to the design of more successful interventions at both the behavioral and pharmacological level.