Literature DB >> 9688586

Ion channels in microglia (brain macrophages).

C Eder1.   

Abstract

Microglia are immunocompetent cells in the brain that have many similarities with macrophages of peripheral tissues. In normal adult brain, microglial cells are in a resting state, but they become activated during inflammation of the central nervous system, after neuronal injury, and in several neurological diseases. Patch-clamp studies of microglial cells in cell culture and in tissue slices demonstrate that microglia express a wide variety of ion channels. Six different types of K+ channels have been identified in microglia, namely, inward rectifier, delayed rectifier, HERG-like, G protein-activated, as well as voltage-dependent and voltage-independent Ca2+-activated K+ channels. Moreover, microglia express H+ channels, Na+ channels, voltage-gated Ca2+ channels, Ca2+-release activated Ca2+ channels, and voltage-dependent and voltage-independent Cl- channels. With respect to their kinetic and pharmacological properties, most microglial ion channels closely resemble ion channels characterized in other macrophage preparations. Expression patterns of ion channels in microglia depend on the functional state of the cells. Microglial ion channels can be modulated by exposure to lipopolysaccharide or various cytokines, by activation of protein kinase C or G proteins, by factors released from astrocytes, by changes in the concentration of internal free Ca2+, and by variations of the internal or external pH. There is evidence suggesting that ion channels in microglia are involved in maintaining the membrane potential and are also involved in proliferation, ramification, and the respiratory burst. Further possible functional roles of microglial ion channels are discussed.

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Year:  1998        PMID: 9688586     DOI: 10.1152/ajpcell.1998.275.2.C327

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  43 in total

1.  A Kv1.5 to Kv1.3 switch in endogenous hippocampal microglia and a role in proliferation.

Authors:  S A Kotecha; L C Schlichter
Journal:  J Neurosci       Date:  1999-12-15       Impact factor: 6.167

2.  Metabotropic glutamate receptor-mediated signaling in neuroglia.

Authors:  David J Loane; Bogdan A Stoica; Alan I Faden
Journal:  Wiley Interdiscip Rev Membr Transp Signal       Date:  2012-01-11

3.  Functional expression of Kir4.1 channels in spinal cord astrocytes.

Authors:  M L Olsen; H Higashimori; S L Campbell; J J Hablitz; H Sontheimer
Journal:  Glia       Date:  2006-04-01       Impact factor: 7.452

4.  Integration of K+ and Cl- currents regulate steady-state and dynamic membrane potentials in cultured rat microglia.

Authors:  Evan W Newell; Lyanne C Schlichter
Journal:  J Physiol       Date:  2005-07-14       Impact factor: 5.182

Review 5.  Blood-brain barrier integrity and glial support: mechanisms that can be targeted for novel therapeutic approaches in stroke.

Authors:  Patrick T Ronaldson; Thomas P Davis
Journal:  Curr Pharm Des       Date:  2012       Impact factor: 3.116

Review 6.  K+ channel modulators for the treatment of neurological disorders and autoimmune diseases.

Authors:  Heike Wulff; Boris S Zhorov
Journal:  Chem Rev       Date:  2008-05       Impact factor: 60.622

7.  Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (I CRAC) but not Ca2+-activated TRPM4-like currents (I CAN) in cultured mouse microglial cells.

Authors:  Andreas Beck; Reinhold Penner; Andrea Fleig
Journal:  J Physiol       Date:  2007-11-08       Impact factor: 5.182

8.  A novel physiological mechanism of glycine-induced immunomodulation: Na+-coupled amino acid transporter currents in cultured brain macrophages.

Authors:  Tom Schilling; Claudia Eder
Journal:  J Physiol       Date:  2004-07-08       Impact factor: 5.182

9.  Immunomodulation of voltage-dependent K+ channels in macrophages: molecular and biophysical consequences.

Authors:  Núria Villalonga; Miren David; Joanna Bielanska; Rubén Vicente; Núria Comes; Carmen Valenzuela; Antonio Felipe
Journal:  J Gen Physiol       Date:  2010-02       Impact factor: 4.086

10.  In vivo and ex vivo evaluation of L-type calcium channel blockers on acid beta-glucosidase in Gaucher disease mouse models.

Authors:  Ying Sun; Benjamin Liou; Brian Quinn; Huimin Ran; You-Hai Xu; Gregory A Grabowski
Journal:  PLoS One       Date:  2009-10-07       Impact factor: 3.240

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