Properties of K
            <sup>+</sup>
            and Cl
            <sup>−</sup>
            channels and their involvement in proliferation of rat microglial cells

Schlichter, Lyanne C.; Sakellaropoulos, G.P.; Ballyk, Barbara A.; Pennefather, Peter; Phipps, David

doi:10.1002/(sici)1098-1136(199607)17:3<225::aid-glia5>3.0.co;2-#

Cited by 136 publications

(164 citation statements)

References 47 publications

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“…The gene encoding this channel is unknown. A chloride current with similar (not identical) biophysical and pharmacological properties was found in cultured microglia cells (Visentin et al, 1995;Schlichter et al, 1996;Eder, 1998). In these cells, it was found to be spontaneously active, although cell swelling, application of physical stretch, or the ramification process all increased its expression.…”

Section: Voltage-gated Chloride Channelsmentioning

confidence: 75%

“…However, a VDAC-like current was found to be a requirement for proliferation in microglia, as blockade of this current was found to decrease proliferation rate (Schlichter et al, 1996). In Schwann cells, the situation is complex and not convincing: Wilson and Chiu (1993) found that DIDS (a broad-spectrum chloride channel inhibitor) exposure enhanced proliferation rates, whereas Pappas and Ritchie (1998) found the opposite.…”

Section: Proliferationmentioning

confidence: 99%

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Chloride/anion channels in glial cell membranes

Walz

2002

Glia

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At least seven different chloride/anion currents have now been identified in astrocytes, oligodendrocytes/Schwann cells, and microglia. Only for two of these currents is the corresponding gene known. One of these genes is not encoding for a chloride channel, but for a class of mitochondria-like pores also found in cell membranes. Astrocytes and oligodendrocytes differ in their resting properties: astrocytes accumulate chloride but do not have a significant permeability. Oligodendrocytes have a close to passive distribution and a significant permeability. Under certain circumstances, astrocytes can express a resting chloride conductance. Reactive and neoplastic astrocytes as well as astrocytes with an altered shape exhibit a resting conductance. The function of these channels certainly involves volume regulation. Other possible functions are potassium homeostasis, migration, proliferation (in microglia), and involvement in spreading depression waves. Of greatest interest are two phenomena discovered in situ: The ClC-2 channel is only found in astrocytic endfeet near blood capillaries adjacent to neuronal GABA A receptors. In the supraoptic nucleus of the hypothalamus, there is an osmosensitive astrocytic taurine release. This released taurine interacts with glycine receptors in neighboring neurons, causing inhibition. It is assumed that with the future availability of more in situ, rather than in vitro, studies, an increased number of such complex interactions between glial cells, neurons, and blood vessels will be discovered.

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Section: Voltage-gated Chloride Channelsmentioning

confidence: 75%

Section: Proliferationmentioning

confidence: 99%

Chloride/anion channels in glial cell membranes

Walz

2002

Glia

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“…This effect was suggested to be a result of cell depolarization since it was duplicated in the presence of increased levels of external K ϩ . Previous work has reported the presence of maxi-conductance type anion channels in excised patches from human microglia (McLarnon et al, 1997) and low conductance anion channels have been documented in rat microglia (Schlichter et al, 1996). Although it is unknown whether either of these Cl Ϫ channels in microglia is blocked by acid pH, anion channels in different tissues have been shown to be sensitive to changes in external pH (Nilius et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of store‐operated Ca²⁺ influx by acidic extracellular pH in cultured human microglia

Khoo

Helm

Choi

et al. 2001

Glia

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The effects of extracellular acidification on Ca 2ϩ -dependent signaling pathways in human microglia were investigated using Ca 2ϩ -sensitive fluorescence microscopy. Adenosine triphosphate (ATP) was used to elicit Ca 2ϩ responses primarily dependent on the depletion of intracellular endoplasmic reticulum (ER) stores, while platelet-activating factor (PAF) was used to elicit responses primarily dependent on store-operated channel (SOC) influx of Ca 2ϩ . The duration of transient responses induced by ATP was not significantly different in standard physiological pH 7.4 (mean duration 30.2 Ϯ 2.5 s) or acidified pH 6.2 (mean duration 31.7 Ϯ 2.8 s) extracellular solutions. However, the time course of the PAF response at pH 7.4 was significantly reduced by 87% with external pH at 6.2. These results suggest that acidification of extracellular solutions inhibits SOC entry of Ca 2ϩ with little or no effect on depletion of ER stores. Changes of extracellular pH over the range from 8.6 to 6.2 during the development of a sustained SOC influx induced by PAF resulted in instantaneous modulation of SOC amplitude indicating a rapidly reversible effect of pH on this Ca 2ϩ pathway. Whole-cell patch clamp recordings showed external acidification blocked depolarization-activated outward K ϩ current indicating cellular depolarization may be involved in the acid pH inhibition. Since SOC mediated influx of Ca 2ϩ is strongly modulated by membrane potential, the electrophysiological data suggest that acidification may act to inhibit SOC by cellular depolarization. These results suggest that acidification observed during cerebral ischemia may alter microglial responses and functions. GLIA 36:22-30, 2001.

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“…This result, coupled with the finding of the inhibition of Ca 2+ influx with raised external K + , suggests that any maneuver which leads to depolarization of human microglia may reduce store-operated influx of Ca 2+ . Since the expression of anion channels has previously been documented in both human [11] and rodent [17] microglia, the present study was designed to study the possible effects of the modulation of such channels on Ca 2+ entry. The clear finding was that replacement of external Cl -by an impermeant anion significantly inhibited entry of Ca 2+ mediated by store-operated channels.…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, previous work has shown the expression of anion currents in both human [11] and rodent [17] microglial membrane.…”

Section: Introductionmentioning

confidence: 92%

Anion channels modulate store-operated calcium influx in human microglia

et al. 2000

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Properties of K ⁺ and Cl ⁻ channels and their involvement in proliferation of rat microglial cells

Cited by 136 publications

References 47 publications

Chloride/anion channels in glial cell membranes

Chloride/anion channels in glial cell membranes

Inhibition of store‐operated Ca²⁺ influx by acidic extracellular pH in cultured human microglia

Anion channels modulate store-operated calcium influx in human microglia

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Properties of K + and Cl − channels and their involvement in proliferation of rat microglial cells

Cited by 136 publications

References 47 publications

Chloride/anion channels in glial cell membranes

Chloride/anion channels in glial cell membranes

Inhibition of store‐operated Ca2+ influx by acidic extracellular pH in cultured human microglia

Anion channels modulate store-operated calcium influx in human microglia

Contact Info

Product

Resources

About

Properties of K ⁺ and Cl ⁻ channels and their involvement in proliferation of rat microglial cells

Inhibition of store‐operated Ca²⁺ influx by acidic extracellular pH in cultured human microglia