Circuit mechanisms of altered excitability in experimental cortical malformations (A06)

• Subject Area: Molecular Biology and Physiology of Neurons and Glial Cells
• Term: since 2017
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 227953431

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.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1089: Synaptic Micronetworks in Health and Disease
• Applicant Institution: Rheinische Friedrich-Wilhelms-Universität Bonn
• Project Heads: Professor Dr. Heinz Beck; Professorin Dr. Susanne Schoch McGovern