In the previous funding period, we identified a transient period of increased excitability in the thalamocortical neuronal network in the course of inflammatory and demyelinating events. Preliminary data point to specific K+ channels, cytokines and components of the kallikrein-kinin system (KKS) as modulators of neuronal hyperexcitability in animal models of multiple sclerosis (MS). In the next funding period, we aim to investigate how the KKS influences MS pathophysiology and to identify the underlying cellular and neuronal network effects. In addition, we aim to establish components of the KKS as possible human biomarkers for different forms of MS and effector channels of KKS signaling as new potential therapeutic targets.
Budde, Thomas | Institute of Physiology I (Neurophysiology) |
Göbel, Kerstin | Department for Neurology |
Budde, Thomas | Institute of Physiology I (Neurophysiology) |
Göbel, Kerstin | Department for Neurology |