Project Details
Projekt
Role of glial Ca2+ signals during neuroinflammation, axonal degeneration, and de- and remyelination in the mouse spinal cord – Part II
Applicants
Professor Dr. Frank Kirchhoff; Dr. Anja Scheller
Subject Area
Molecular and Cellular Neurology and Neuropathology
Term
from 2015 to 2023
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 262890264
While neuronal network function is largely encoded by distinct patterns of action potential firing, glial cell functions are determined by a complex temporal and spatial arrangement of Ca2+ signals. Dysregulation of Ca2+ is a common phenomenon of neuroinflammatory diseases, including multiple sclerosis (MS). Experimental autoimmune encephalomyelitis (EAE) and toxic cuprizone-evoked demyelination are two animal models that mimic different components (e.g. inflammation or remyelination) of the human disease. Using in vivo twophoton laser-scanning microscopy (2P-LSM) and genetically modified mice with cell-specific genetically encoded Ca2+ indicator expression we will analyse spontaneous and evoked Ca2+ signals of oligodendrocytes, astrocytes and microglia within the dorsal spinal tracts in both MS models. Identification of the underlying molecular pathways in vivo will help to understand the complex pathomechanisms of MS and will provide novel options for the development of therapeutic strategies.
DFG Programme
Research Units
