The potassium channels Kv1.5 and Kv1.3 modulate distinct functions of microglia

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Item Type:	Article
Title:	The potassium channels Kv1.5 and Kv1.3 modulate distinct functions of microglia
Creators Name:	Pannasch, U., Faerber, K., Nolte, C., Blonski, M., Yan Chiu, S., Messing, A. and Kettenmann, H.
Abstract:	Activation of microglia by LPS leads to an induction of cytokine and NO release, reduced proliferation and increased outward K(+) conductance, the latter involving the activation of Kv1.5 and Kv1.3 channels. We studied the role of these channels for microglial function using two strategies to interfere with channel expression, a Kv1.5 knockout (Kv1.5(-/-)) mouse and an antisense oligonucleotide (AO) approach. The LPS-induced NO release was reduced by AO Kv1.5 and completely absent in the Kv1.5(-/-) animal; the AO Kv1.3 had no effect. In contrast, proliferation was augmented with both, loss of Kv1.3 or Kv1.5 channel expression. After facial nerve lesion, proliferation rate was higher in Kv1.5(-/-) animals as compared to wild type. Patch clamp experiments confirmed the reduction of the LPS-induced outward current amplitude in Kv1.5(-/-) microglia as well as in Kv1.5- or Kv1.3 AO-treated cells. Our study indicates that induction of K(+) channel expression is a prerequisite for the full functional spectrum of microglial activation.
Keywords:	Brain, Bromodeoxyuridine, Cell Proliferation, Cultured Cells, Chemokines, Cytokines, Radiation Dose-Response Relationship, Electric Stimulation, Mammalian Embryo, Facial Nerve Diseases, Immunohistochemistry, Kv1.3 Potassium Channel, Kv1.5 Potassium Channel, Lipopolysaccharides, Membrane Potentials, Inbred C57BL Mice, Knockout Mice, Microglia, Nitric Oxide, Antisense Oligodeoxyribonucleotides, Patch-Clamp Techniques, Reverse Transcriptase Polymerase Chain Reaction, Animals, Mice
Source:	Molecular and Cellular Neuroscience
ISSN:	1044-7431
Publisher:	Academic Press
Volume:	33
Number:	4
Page Range:	401-411
Date:	15 December 2006
Official Publication:	https://doi.org/10.1016/j.mcn.2006.08.009
PubMed:	View item in PubMed

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