Functional role of endogenous Kv1.4 in experimental demyelination
Gonzalez Alvarado M, Rötger C, Berger L, London B, Haase S, Kuhbandner K, Lee DH, Linker RA (2020)
Publication Type: Journal article
Publication year: 2020
Journal
Book Volume: 343
Article Number: 577227
DOI: 10.1016/j.jneuroim.2020.577227
Abstract
During neuroinflammation, the shaker type potassium channel Kv1.4 is re-expressed in oligodendrocytes (Ol), but not immune cells. Here, we analyze the role of endogenous Kv1.4 in two demyelinating animal models of multiple sclerosis. While Kv1.4 deficiency in primary murine Ol led to a decreased proliferation rate in vitro, it did not exert an effect on Ol proliferation or on the extent of de- or remyelination in the cuprizone model in vivo. However, in experimental autoimmune encephalomyelitis, Kv1.4−/− mice exhibited a milder disease course and reduced Th1 responses. These data argue for an indirect effect of Kv1.4 on immune cells, possibly via glial cells.
Authors with CRIS profile
Maria Gonzalez Alvarado
Department of Neurology
Caroline Rötger
Department of Neurology
Laura Berger
Department of Neurology
Kristina Kuhbandner
Department of Neurology
Involved external institutions
Germany (DE)
United States (USA) (US)How to cite
APA:
Gonzalez Alvarado, M., Rötger, C., Berger, L., London, B., Haase, S., Kuhbandner, K.,... Linker, R.A. (2020). Functional role of endogenous Kv1.4 in experimental demyelination. Journal of Neuroimmunology, 343. https://doi.org/10.1016/j.jneuroim.2020.577227
MLA:
Gonzalez Alvarado, Maria, et al. "Functional role of endogenous Kv1.4 in experimental demyelination." Journal of Neuroimmunology 343 (2020).
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