Cholinergic agonists increase intracellular Ca2+ in cultured human microglia

Zhang, Lili; McLarnon, James G.; Goghari, Vikram; Lee, Yong Beom; Kim, Seung Up; Krieger, Charles

doi:10.1016/s0304-3940(98)00706-x

Cited by 33 publications

(26 citation statements)

References 13 publications

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“…The first evidence for functional SOCE in microglial cells was obtained by [Ca 2ϩ ] imaging experiments investigating the response of microglia to complement fragments or endothelin (603,605 (326,573,982,985,1031). However, the SOCE in human microglia is not only coupled to P2Y purinoceptor-dependent depletion of internal stores, but is also modulated by membrane depolarization either following the activation of Cl Ϫ channels (570) or ionotropic P2X purinoceptors (568).…”

Section: B Store-operated Ca 2؉ Entrymentioning

confidence: 99%

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Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,134

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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Section: B Store-operated Ca 2؉ Entrymentioning

confidence: 99%

“…In cultured microglial cells from the human brain, application of carbachol triggered cytosolic [Ca 2ϩ ] i transients, which were blocked by atropine and originated from Ca 2ϩ release from the ER, thus suggesting functional expression of muscarinic cholinoreceptors (990,1031).…”

Section: Cholinergic Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,134

2,981

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“…Recently, we have also found that carbachol acts in the same manner as ATP in eliciting increased [Ca 2ϩ ] i in human microglia. 40 …”

Section: Effects Of Atp On Intracellular Ca 2ϩmentioning

confidence: 99%

Effects of ATP and elevated K+ on K+ currents and intracellular Ca2+ in human microglia

et al. 1999

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“…Among the spectrum of stimuli found to elicit transient Ca 2+ responses in cultured rodent cells are complement [1], ATP [2][3][4], carbachol [5], platelet-activating factor (PAF [6]) and endothelin [7]. All of these stimuli (complement has not yet been tested) have also been found to cause transient Ca 2+ responses in human microglia [8][9][10][11]. It is important to note that differences between properties of rodent and human microglia have been reported such as the expression of inducible NOS by rodent, but not human, microglia [12].…”

Section: Introductionmentioning

confidence: 99%