Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 24, Issue 3-4, Pages 141-152Publisher
KARGER
DOI: 10.1159/000233240
Keywords
Microglia; Brain macrophage; Potassium channels; Kv1.3; Kir2.1; Margatoxin; Patch-clamp
Categories
Funding
- Boehringer Ingelheim
Ask authors/readers for more resources
Microglia are the intrinsic immune cells of the brain. As such, they are crucially involved in neuro-protection as well as neuro-degeneration. Their activation leads to the induction of cytokine and chemokine release, the production of reactive oxygen species and nitric oxide and an increased outward potassium conductance. In this study, we focus our interest on potassium currents and channels in the C8-B4 murine microglial cell line and compare them with those of primary cultured microglia from neo-natal mice. Using the whole cell patch-clamp technique, we have recorded prominent inward and outward rectifying voltage-dependent potassium currents but no calcium-activated potassium currents. Using pharmacological, biophysical and molecular approaches, we demonstrate that Kv1.3 and Kir2.1 channels underlie outward and inward rectifying potassium currents, respectively. In contrast to primary cultured microglia, we observe that an outward rectifying potassium current is already present in unstimulated C8-B4 cells. However, as seen in primary microglia, this current increases after treatment with LPS, IFN-gamma, TGF-beta and GM-CSF and is suppressed by treatment with protein kinase inhibitors. Our study indicates that the C8-B4 cell line shows similar though not identical potassium channel properties compared to primary cultured microglia. We demonstrate that despite some differences, they are a useful tool to study potassium currents in microglial activation mechanisms by means of electrophysiological methods without the need for preparation of cells as primary culture. Copyright (C) 2009 S. Karger AG, Basel
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available