3 articles published in JoVE
An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices Kerstin Göbel1, Stefan Bittner1,2, Manuela Cerina3, Alexander M. Herrmann1, Heinz Wiendl1, Sven G. Meuth1,3 1Department of Neurology, University of Münster, 2Germany and Interdisciplinary Center for Clinical Research (IZKF) Münster, 3Institute of Physiology I - Neuropathophysiology I, University of Münster To address mechanisms of demyelination and neuronal apoptosis in cortical lesions of inflammatory demyelinating disorders, different animal models are used. We here describe an ex vivo approach by using oligodendrocyte-specific CD8+ T-cells on brain slices, resulting in oligodendroglial and neuronal death. Potential applications and limitations of the model are discussed.
Isolation of Primary Murine Brain Microvascular Endothelial Cells Tobias Ruck1, Stefan Bittner1,2, Lisa Epping1, Alexander M. Herrmann1, Sven G. Meuth1,3 1Department of Neurology, University of Münster, 2Interdisciplinary Center for Clinical Research (IZKF) Münster, 3Institute of Physiology I — Neuropathophysiology I, University of Münster Brain microvascular endothelial cells (BMEC) are interconnected by specific junctional proteins forming a highly regulated barrier separating blood and the central nervous system (CNS), the so-called blood-brain-barrier (BBB). The isolation of primary murine brain microvascular endothelial cells, as discussed in this protocol, enables detailed in vitro studies of the BBB.
Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice Stefan Bittner1,2, Ali M. Afzali1, Heinz Wiendl1, Sven G. Meuth1,3 1Department of Neurology, University of Münster, 2Interdisciplinary Center for Clinical Research (IZKF), Münster, 3Institute of Physiology – Neuropathophysiology, University of Münster Experimental autoimmune encephalomyelitis (EAE) is an established animal model of multiple sclerosis. C57BL/6 mice are immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 (MOG35-55), resulting in an ascending flaccid paralysis caused by autoreactive immune cells in the central nervous system. Protocols for disease induction and monitoring will be discussed.