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Cell Calcium. 2004 May;35(5):449-59.

Inwardly rectifying K+ channels influence Ca2+ entry due to nucleotide receptor activation in microglia.

Author information

1
Laboratory of Organ and System Pathophysiology, Department of Cell Biology and Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.

Abstract

The expression in microglia of two K+ channel populations, inwardly- and delayed outwardly rectifying channels (Kir, Kdr), is under the control of a variety of signals among which inflammatory and immunomodulatory agents. This makes K+ channels good candidates for the control of cell activities and for their adaptation to the changes of the functional state of the cell. Here we investigated on the role played by Kir channels in the control of cytoplasmic Ca2+ movements. In particular, we focused on those linked to nucleotide receptors, which are known to regulate a variety of functions in microglia. By a Fura-2-based video-imaging approach we recorded Ca2+ transients induced by P2 activation. These were composed of an initial peak, mainly due to release from endoplasmic reticulum, and of a long lasting plateau linked to Ca2+ influx through cation non-selective and capacitative channels. In patch-clamp experiments, we observed that Ba2+ (1-100 microM) could inhibit Kir current, but was not effective on Kdr and ATP-induced K+ current. By using Ba2+ as a specific blocker of Kir channels, we found that their inhibition caused a decrease of the Ca2+ level, especially at the end of the 20s long agonist application period. The effect of Ba2+ was mimicked by high K(+)-induced depolarization. We conclude that Kir channels contribute to modulate the amplitude and time course of the ATP-induced Ca2+ transient through the control of membrane potential. We suggest that microglial cells adapt signal transduction mechanisms to the changes of their functional state also by varying the expression and modulating the activity of inwardly rectifying K+ channels.

PMID:
15003854
DOI:
10.1016/j.ceca.2003.11.001
[Indexed for MEDLINE]

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