Characterization and regulation of rat microglial Ca2+ release-activated Ca2+ (CRAC) channel by protein kinases

Hahn, Junghyun; Jung, Wonyong; Kim, Namin; Uhm, Dae-Yong; Chung, Sungkwon

doi:10.1002/1098-1136(200008)31:2<118::aid-glia30>3.0.co;2-0

Cited by 29 publications

(10 citation statements)

References 40 publications

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“…At the mammalian NMJ, the activation of PKA and PKC has opposite effects on postsynaptic nAChR stability, and this contributes to synaptic stabilization or elimination (Nelson et al,2003,2005). Opposite effects of PKC and PKA have been observed in such other cell activities as the immunity cells function (Hermann‐Kleiter et al,2006), cell proliferation (Fortino et al,2002), expression of glial proteins (Hahn et al,2000), and renal cell function (Stark et al,1998).…”

Section: Discussionmentioning

confidence: 99%

Interaction between protein kinase C and protein kinase A can modulate transmitter release at the rat neuromuscular synapse

Santafé

García

Lanuza

et al. 2008

J of Neuroscience Research

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We used intracellular recording to investigate the functional interaction between protein kinase C (PKC) and protein kinase A (PKA) signal transduction cascades in the control of transmitter release in the neuromuscular synapses from adult rats. Our results indicate that: 1) PKA and PKC are independently involved in asynchronous release. 2) Evoked acetylcholine (ACh) release is enhanced with the PKA agonist Sp-8-BrcAMP and the PKC agonist phorbol ester (PMA). 3) PKA has a constitutive role in promoting a component of normal evoked transmitter release because, when the kinase is inhibited with H-89, the release diminishes. However, the PKC inhibitor calphostin C (CaC) does not affect ACh release. 4) PKA regulates neurotransmission without PKC involvement because, after PMA or CaC modulation of the PKC activity, coupling to the ACh release of PKA can normally be stimulated with Sp-8-BrcAMP or inhibited with H-89. 5) After PKA inhibition with H-89, PKC stimulation with PMA (or inhibition with CaC) does not lead to any change in evoked ACh release. However, in PKA-stimulated preparations with Sp-8-BrcAMP, PKC becomes tonically active, thus potentiating a component of release that can now be blocked with CaC. In normal conditions, therefore, PKA was able to modulate ACh release independently of PKC activity, whereas PKA stimulation caused the PKC coupling to evoked release. In contrast, PKA inhibition prevent PKC stimulation (with the phorbol ester) and coupling to ACh output. There was therefore some dependence of PKC on PKA activity in the fine control of the neuromuscular synaptic functionalism and ACh release.

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Section: Discussionmentioning

confidence: 99%

Interaction between protein kinase C and protein kinase A can modulate transmitter release at the rat neuromuscular synapse

Santafé

García

Lanuza

et al. 2008

J of Neuroscience Research

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“…PKA may in turn phosphorylate and activate several types of Ca 21 channels including the Ca 21 release-activated Ca 21 (CRAC) channels, a kind of highly Ca 21 -selective SOCs (Hahn et al, 2000;Rossie, 1999;Wu et al, 1999). We found that blockade of PKA with its specific antagonist, H-89, significantly attenuated the effect of NaHS, suggesting that activation of cAMP/PKA pathway may open Ca 21 channels such as CRAC channels and therefore increase [Ca 21 ] i .…”

Section: Discussionmentioning

confidence: 99%

“…Intracellular calcium could be regulated by different signaling pathways such as cAMP/cAMP-dependent protein kinase (PKA) (Hahn et al, 2000;Rossie, 1999;Wu et al, 1999) and phospholipase C (PLC)/protein kinase C (PKC)/phosphoinositol-3,4,5-inositol (IP 3 ) (Bian et al, 1998a) cascades. Previously, it has been found that H 2 S activates cAMP/PKA pathway in both neuronal and glial cells (Kimura, 2000).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen sulphide regulates calcium homeostasis in microglial cells

Lee¹,

Hu²,

Hu³

et al. 2006

Glia

135

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Hydrogen sulphide (H 2 S), which is produced endogenously from L-cysteine in mammalian tissues, has been suggested to function as a neuromodulator in the brain. However, the role of H 2 S in microglial cells is unclear. In this study, the effect of exogenous and endogenous H 2 S on intracellular calcium homeostasis was investigated in primary cultured microglial cells. Sodium hydrosulphide (NaHS), a H 2 S donor, caused a concentration-dependent (0.1-0.5 mM) increase in intracellular calcium concentration ([Ca 21 ] i ). This effect was significantly attenuated in the presence of a calcium-free extracellular solution, Gd 31 (100 lM), a nonselective Ca 21 channel blocker, or thapsigargin (2 lM), an inhibitor of the sarcoplasmic/endoplasmic reticulum Ca 21 -ATPase. These observations suggest that the increase in [Ca 21 ] i in response to H 2 S involves both calcium influx across the plasma membrane and calcium release from intracellular stores. The H 2 S-induced calcium elevation is partly attenuated by H-89, a selective cAMP-dependent protein kinase (PKA) inhibitor, but not by U73122, a phospholipase C (PLC) inhibitor, and chelerythrine, a selective protein kinase C (PKC) inhibitor, suggesting the involvement of cAMP/PKA, but not PLC/PKC/phosphoinositol-3,4,5-inositol (IP 3 ) pathway. Using RT-PCR, only cystathionine g-lyase (CSE), a H 2 S producing enzyme, was detected in primary cultures of microglia. Lowering endogenous H 2 S level with, D,L-propargylglycine and b-cyano-L-alanine, two CSE inhibitors, significantly decreased [Ca 21 ] i , suggesting that endogenous H 2 S may have a positive tonic influence on [Ca 21 ] i homeostasis. These findings support the possibility that H 2 S may serve as a neuromodulator to facilitate signaling between neurons and microglial cells.

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“…CRAC currents in microglia exhibit strong inward rectification. A single‐channel conductance of 42 pS was determined for microglial CRAC channels carrying Na + (Nörenberg et al, 1997; Hahn et al, 2000). CRAC channels are inhibited by Gd 3+ or La 3+ in the nanomolar concentration range (Lewis, 2001).…”

Section: Regulation Of Intracellular Ion Concentrationsmentioning

confidence: 99%

Regulation of microglial behavior by ion channel activity

Eder

2005

J of Neuroscience Research

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Microglia play an important role in the central nervous system, where these cells, it is believed, have both neuroprotective and neurotoxic effects. In response to acute brain injury or during neurodegenerative and neuroinflammatory diseases, activated microglial cells undergo shape changes, migrate to the affected sites of neuronal damage, proliferate, and release a variety of substances, such as cytokines and reactive oxygen species (ROS). This review summarizes the physiological mechanisms underlying microglial activation and deactivation processes, with particular focus on the involvement of microglial ion channels. Microglial ion channels have been shown to be capable, by regulating membrane potential, cell volume, and intracellular ion concentrations, of modulating or facilitating proliferation, migration, cytokine secretion, shape changes, and the respiratory burst of microglial cells.

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Characterization and regulation of rat microglial Ca2+ release-activated Ca2+ (CRAC) channel by protein kinases

Cited by 29 publications

References 40 publications

Interaction between protein kinase C and protein kinase A can modulate transmitter release at the rat neuromuscular synapse

Interaction between protein kinase C and protein kinase A can modulate transmitter release at the rat neuromuscular synapse

Hydrogen sulphide regulates calcium homeostasis in microglial cells

Regulation of microglial behavior by ion channel activity

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