Successful social functioning requires quick and accurate processing of emotion and generation of appropriate reactions. In typical individuals, these skills are supported by embodied processing, recruiting central and peripheral mechanisms. However, emotional processing is atypical in individuals with autism spectrum disorder (ASD). Individuals with ASD show deficits in recognition of briefly presented emotional expressions. They tend to recognize expressions using rule-based, rather than template, strategies. Individuals with ASD also do not spontaneously and quickly mimic emotional expressions, unless the task encourages (...) engagement. When processing emotional scenes, ASD individuals show atypical basic motivational responses, despite intact ability to verbally determine stimulus valence. We discuss how these findings highlight the contribution of both embodied and disembodied mechanisms to typical and atypical emotional functioning. (shrink)

Cook et al. argue that mirror neurons originate from associative learning processes, without evolutionary influence from social-cognitive mechanisms. We disagree with this claim and present arguments based upon cross-species comparisons, EEG findings, and developmental neuroscience that the evolution of mirror neurons is most likely driven simultaneously and interactively by evolutionarily adaptive psychological mechanisms and lower-level biological mechanisms that support them.

The target article discusses a model of how brain circuits mediate social behaviors such as imitation and mindreading. Hurley suggests potential mechanisms for development of shared circuits. We propose that empirical studies can be designed to differentiate the influence of genetic and learning-based factors on the development of shared circuits. We use the mirror neuron system as a model system.