Mechanisms and consequences of a defect redox control of Kv4.3 channels in Morbus Parkinson
(A13)
Subject Area
Molecular Biology and Physiology of Neurons and Glial Cells
Anatomy and Physiology
Term
from 2009 to 2020
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 61867463
We aim to clarify the mechanisms that lead to an altered redox-state of Kv4.3 potassium channels and in turn to hyperactivity in dopamine substantia nigra (DA SN) neurons in a transgenic mutant alpha-synuclein mouse model of Parkinson disease (PD). By comparison with a CRISP/Cas-mediated redox-insensitive Kv4.3 mutant (C110), we aim to define the causal role of redox-mediated hyperactivity for selective neurodegeneration of DA SN neurons in PD.
DFG Programme
Collaborative Research Centres
