Functional role of endogenous Kv1.4 in experimental demyelination

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. [Display omitted] •Kv1.4 deficiency decreases oligodendrocyte proliferation in vitro.•Deficiency of Kv1.4 does not impact remyelination in vivo.•Lack of Kv1.4 influences T cell cytokine release and ameliorates the course of EAE.