Bateup will use genetic mouse models of ASD to investigate the idea that synaptic alterations in the striatum are central to the inflexible behaviors observed in ASD.

Polimanti will use genetic- and brain-imaging approaches to understand the relationship between positive selection for common ASD risk alleles and cognitive abilities in affected and unaffected individuals.

Tsai will delineate contributions of cerebellar dysfunction to autism-related behaviors in mice and assess benefits of cerebellar neuromodulation to treat these behaviors.

The molecular and circuit underpinnings of repetitive behavior dysfunction — a core symptom of ASD — have remained elusive, but it is assumed that they rely on the same basal ganglia circuits that underlie repetitive behavior control and habit formation. The current project aims to investigate, with unprecedented spatial and temporal resolution, the circuit alterations in the striatum that lead to alterations in spontaneous and learned behavioral sequences in ASD.

Frick previously demonstrated a link between BKCa channel dysfunction, neocortical hyperexcitability and sensory hypersensitivity in the Fmr1-/y model of ASD. Drawing on this work, Frick will explore the potential of channel agonists for the therapeutic correction of phenotypes associated neocortical hyperexcitability/sensory hypersensitivity in genetic mouse models of ASD.

Choi proposes to use the MIA mouse model with a discrete, functionally relevant lesion in the primary somatosensory cortex to elucidate neural circuits that modulate ASD-associated behaviors.