Autism is a neurodevelopmental disorder for which diagnosis is based on three domains of behavioral symptoms: (1) abnormal social interactions, (2) impaired communication, and (3) repetitive behaviors. Currently, the only treatments that effectively improve these core symptoms are behavioral interventions implemented at early ages (Vismara and Rogers, 2010). Although pharmacological treatments are available for associated symptoms, including self-injury, tantrums, aggression, and seizures, considerable research is needed to discover pharmacological targets for the diagnostic domains.

Mouse models of autism spectrum disorders provide translational research tools for understanding the causes of autism spectrum disorders and for developing treatments (Ehninger et al, 2008; Silverman et al, 2010). We are interested in the mechanisms that underlie improvements in autism-relevant behavioral phenotypes in genetic mouse models. Given the effectiveness of early behavioral therapies for reducing symptoms in autism, we reasoned that behavioral interventions might similarly rescue social and/or repetitive abnormalities in mouse models. To test this hypothesis, we used an inbred strain of mice, BTBR T+tf/J (BTBR), which displays low sociability on multiple social tasks, reduced ultrasonic vocalizations and behavioral responses to olfactory social cues, and high-repetitive self-grooming. BTBR were given opportunities to interact with C57BL/6J (B6), an inbred strain with high-sociability and low-repetitive behaviors.

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