Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells.

Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells. Research Abstract Details 

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Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells. Abstract Text:

Andreas Beck,Reinhold Penner,Andrea Fleig,Andreas Beck,Reinhold Penner,Andrea Fleig,

Microglia are the main immunocompetent cells of the mammalian central nervous system (CNS). Activation of cultured microglial cells and subsequent release of nitric oxide and cytokines critically depends on intracellular calcium levels. Since microglia undergo dramatic morphological, biochemical and electrophysiological changes in response to pathological events in the CNS, we investigated temporal changes in expression levels of ion channels involved in cellular calcium homeostasis in mouse cortical microglial cells in culture. Specifically, we assessed the inward and delayed outward rectifier potassium currents (I(IRK) and I(DRK)), calcium (Ca(2+)) release-activated Ca(2+) currents (I(CRAC)) and Ca(2+)-activated TRPM4-like currents (I(CAN)) in non-activated microglia and cells that were activated by exposure to lipopolysaccharide (LPS) between 3 and 48 h. Unstimulated microglial cells, subcultured from an astrocyte coculture, typically exhibited a ramified, rod-shaped morphology. During the first 3 days of culture cell size and shape were maintained, but the percentage of cells showing prominent I(IRK) went up and those expressing I(DRK) went down. Cells retaining I(DRK) exhibited smaller amplitudes, whereas those of I(IRK) and I(CRAC) were not affected. However, after 24 h of exposure to 1 mug ml(-1) LPS, most cells showed an amoeboid ('fried egg'-shaped) morphology with a 62% increase in cell capacitance. At that point in time, only 14% of the cells revealed I(IRK) and 3% had I(DRK) exclusively, whereas the majority of cells expressed both currents. The amplitudes of I(CRAC) and I(IRK) progressively decreased after stimulation, whereas I(DRK) transiently reached a maximum after 6 h of LPS exposure and then returned to pre-stimulation expression levels. Cultured microglia also revealed TRPM4-like, Ca(2+)-activated non-selective currents (I(CAN)) with an EC(50) of 1.2 mum [Ca(2+)](i). The expression levels of this current did not change significantly during and after 24 h of LPS exposure. We propose that LPS-induced down-regulation of I(IRK) and I(CRAC) will reduce the cell's capacity to produce significant calcium influx upon receptor activation and result in decreased sensitivity to exogenous stimulation. In this scenario, I(CAN) expression would remain constant, although its activity would automatically be reduced due to the diminished calcium influx capacity of the cell.

Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells. Publishing Authors By Initials

A Beck,R Penner,A Fleig,A Beck,R Penner,A Fleig,

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Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of physiology

VOLUME: 586

Page Numbers: 427-39

Journal Abbreviation: J. Physiol. (Lond.)

ISSN: 0022-3751

DAY: 8

MONTH: 11

YEAR: 2007

Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (ICRAC) but not Ca2+-activated TRPM4-like currents (ICAN) in cultured mouse microglial cells.

AFFILIATION: Queen's Center for Biomedical Research, Laboratory of Cell and Molecular Signalling, The Queen's Medical Center and John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. abeck@queens.org.

Country: England

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MEDLINETA: J Physiol

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