Our aim is to understand the role of the sodium channel subtype Nav1.9 in pain syndroms. Fibroblasts from patients with hereditary pain syndromes due to Nav1.9 mutations will be reprogrammed into hiPSC and differentiated to nociceptors. Using electrophysiological and molecular methods, we will monitor the development of excitability in these neurons in order to understand mechanisms of nociception and the role of Nav1.9 in the development of human pain.
IZKF Junior Research Group 3
Department of Anaesthesiology