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

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 interfe...

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Vydáno v:	Molecular and cellular neuroscience Ročník 33; číslo 4; s. 401 - 411
Hlavní autoři:	Pannasch, Ulrike, Färber, Katrin, Nolte, Christiane, Blonski, Mary, Yan Chiu, Shing, Messing, Albee, Kettenmann, Helmut
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Elsevier Inc 15.12.2006
Témata:	Animals Brain - cytology Bromodeoxyuridine - metabolism Cell Proliferation - drug effects Cells, Cultured Chemokines - metabolism Cytokines - metabolism Dose-Response Relationship, Radiation Electric Stimulation - methods Embryo, Mammalian Facial Nerve Diseases - metabolism Facial Nerve Diseases - pathology Immunohistochemistry - methods Kv1.3 Potassium Channel - chemistry Kv1.3 Potassium Channel - physiology Kv1.5 Potassium Channel - chemistry Kv1.5 Potassium Channel - genetics Kv1.5 Potassium Channel - physiology Lipopolysaccharides - pharmacology Membrane Potentials - drug effects Membrane Potentials - physiology Membrane Potentials - radiation effects Mice Mice, Inbred C57BL Mice, Knockout Microglia - drug effects Microglia - physiology Nitric Oxide - metabolism Oligodeoxyribonucleotides, Antisense - pharmacology Patch-Clamp Techniques - methods Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism
ISSN:	1044-7431, 1095-9327
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Shrnutí:	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.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1044-7431 1095-9327
DOI:	10.1016/j.mcn.2006.08.009