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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-
(TGF-) for 24 h. In contrast, inward
rectifier K+ channel expression was unchanged by TGF-.
DR current density was more than sixfold larger in TGF--treated
microglia than in untreated microglia. DR currents of TGF--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 
-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-.
brain macrophages; transforming growth factor-; inward rectifier
K+ current; delayed rectifier K+ current; reverse transcription-polymerase chain reaction; Kir2.1
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