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Am J Physiol Cell Physiol 279: C1123-C1134, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 4, C1123-C1134, October 2000

Upregulation of Kv1.3 K+ channels in microglia deactivated by TGF-beta

Tom Schilling1, Fred N. Quandt2, Vladimir V. Cherny2, Wei Zhou2, Uwe Heinemann1, Thomas E. Decoursey2, and Claudia Eder1

1 Institut für Physiologie der Charité, Humboldt Universität, D 10117 Berlin, Germany; and 2 Department of Molecular Biophysics and Physiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612

Microglial activation is accompanied by changes in K+ channel expression. Here we demonstrate that a deactivating cytokine changes the electrophysiological properties of microglial cells. Upregulation of delayed rectifier (DR) K+ channels was observed in microglia after exposure to transforming growth factor-beta (TGF-beta ) for 24 h. In contrast, inward rectifier K+ channel expression was unchanged by TGF-beta . DR current density was more than sixfold larger in TGF-beta -treated microglia than in untreated microglia. DR currents of TGF-beta -treated cells exhibited the following properties: activation at potentials more positive than -40 mV, half-maximal activation at -27 mV, half-maximal inactivation at -38 mV, time dependent and strongly use-dependent inactivation, and a single channel conductance of 13 pS in Ringer solution. DR channels were highly sensitive to charybdotoxin (CTX) and kaliotoxin (KTX), whereas alpha -dendrotoxin had little effect. With RT-PCR, mRNA for Kv1.3 and Kir2.1 was detected in microglia. In accordance with the observed changes in DR current density, the mRNA level for Kv1.3 (assessed by competitive RT-PCR) increased fivefold after treatment of microglia with TGF-beta .

brain macrophages; transforming growth factor-beta ; inward rectifier K+ current; delayed rectifier K+ current; reverse transcription-polymerase chain reaction; Kir2.1


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