Susanne Schmid will establish systematic and objective measures of sensory processing on the brain-stem level and on the cortical (perceptual) level that can be utilized in both children with ASD and a rodent model of ASD. Schmid expects that the development of these measures will provide better tools for diagnosing sensory-processing difficulties and will provide mechanistic insights that can aid in the development of pharmacological and behavioral treatments.

Ellen Hoffman and Ted Abel aim to compare findings from high-throughput behavior-based screens in zebrafish models of ASD risk genes to mouse behavioral phenotypes in order to elucidate the cellular and circuit-level effects of drug candidates that suppress ASD-relevant behaviors in both systems. The results are expected to identify novel pharmacological targets for further evaluation in ASDs.

Mark Zylka will test the hypothesis that exposure to environmental risk factors for ASD amplifies the effects of genetic risk factors, by assessing the effects of prenatal exposure to a pyrethroid pesticide in a genetic mouse model of ASD (Chd8+/- mice). The results of this research could identify an avoidable environmental risk for a common genetic subtype of autism.

Using a battery of cutting-edge approaches, Song-Hai Shi will investigate lineage-dependent, precise, local and long-range cortical neuron circuit assembly in the Fmr1 knockout mouse model of fragile X syndrome.

Rebecca Saxe will test whether midbrain dopaminergic signals of social cravings, previously observed in mice, are similarly observed in humans. As impairments in social motivation have been postulated to be a core social deficit in autism spectrum disorder (ASD), these results will improve the value of the mouse model for testing mechanisms of altered social motivation in ASD.

Mark Blumberg will perform behavioral and neurophysiological assessments in 16p11.2 deletion mice to determine whether the early sensorimotor and sleep disturbances observed in autism have a common link.