A06 Circuit mechanisms of altered excitability in experimental cortical malformations
This project will address the pathogenesis of the most commonly occurring and severe focal epileptogenic lesions, focal cortical dysplasias and glioneuronal tumors. It will address the role of Ste20-like kinase (SLK), a protein that exhibits decreased expression levels in neurons located in focal lesions in these disorders. Decreased levels of SLK in excitatory neurons of mouse cortex were shown to result in a profound and selective reduction of a specific inhibitory circuit, feed-forward thalamocortical inhibition. In a collaboration between the Schoch and Beck labs, the Ph.D. student will address the consequences of circuit-specific disruption of inhibition for cortical neuronal activity in-vivo during sensorimotor driven behavior.