The Department of Physiology welcomes Dr. Helen Bateup, assistant professor, with University of California, Berkeley.
Abstract:
The basal ganglia comprise a group of sub-cortical nuclei responsible for a variety of functions including motor control, action selection, habit formation, and reward learning. Alterations in basal ganglia circuits are known to give rise to several neurological and psychiatric diseases. Recently, there has been mounting evidence that altered synaptic function within the striatum, the main input center of the basal ganglia, may also be a key pathophysiology in autism spectrum disorder (ASD). Our lab has shown that cell type-specific disruption of autism risk genes in striatal and dopamine neurons is sufficient to induce changes in motor learning, goal-directed behaviors, and cognitive flexibility. We have demonstrated that mutations in ASD-risk genes affect various aspects of striatal and dopaminergic physiology including cell and spine morphology, synaptic plasticity, and neurotransmitter release. Together this work highlights striatal synapses and basal ganglia circuits as important drivers of ASD-related behavioral changes and suggests a potential locus for intervention.