Cholinergic agonists increase intracellular Ca2+ in cultured human microglia
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Acknowledgements
This work was supported by grants from the British Columbia Health Research Foundation (to C.K.), the Natural Science and Engineering Research Council of Canada (to J.G.M.), and the MS Society of Canada (to S.U.K).
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2020, Neuroscience LettersCitation Excerpt :The presence and function of mACh receptors on microglia is poorly documented. Using mAChRs agonists in cultured microglia, two groups reported a transient increase in intracellular Ca2+ [46,47]. Additionally, a flow cytometry analysis of mouse adult brain identified a M3-positive subpopulation representing around 15 % of the microglial cells [8].
Chronic hM3Dq signaling in microglia ameliorates neuroinflammation in male mice
2020, Brain, Behavior, and ImmunityCitation Excerpt :Microglia have been reported to express the α3, α5, α6, α7 and β4 nicotinic channel subunits (Liu et al., 2009; Rock et al., 2008; Shytle et al., 2004; Suzuki et al., 2006). Expression of muscarinic receptors on cultured microglia has also been demonstrated (Pannell et al., 2016; Zhang et al., 1998). In cultured microglia, acetylcholine seems to exert mainly an anti-inflammatory effect on microglia.
Microglial calcium signaling in the adult, aged and diseased brain
2013, Cell CalciumCitation Excerpt :In the brain, acetylcholine is involved in many aspects of behavioral and physiological regulation, e.g. sensory processing, learning, memory, and mood [59]. Microglial cells in vitro express functional metabotropic (muscarinic) acetylcholine receptors (mAChR), because the agonist of mAChRs carbachol (100 μM) as well as acetylcholine (100 μM) evoked an increase in [Ca2+]i in a fraction of cultured human and rat microglia [55,60]. In both preparations, carbachol-induced transients persisted in the Ca2+-free solution and were therefore mediated by Ca2+ release from the intracellular Ca2+ stores.
Microglial calcium signal acts as a rapid sensor of single neuron damage in vivo
2011, Biochimica et Biophysica Acta - Molecular Cell ResearchCitation Excerpt :A smaller fraction (29%; 2/7 cells) responded to prolonged application of the agonist of metabotropic glutamate receptors, trans-ACPD. Other drugs/treatments, which were shown to induce microglial Ca2+ signals in vitro (e.g., cholinergic agonists [46,47], fractalkine [48], and depolarization of the cell membrane [49]), were ineffective (Fig. 4C). Because fractalkine is released by the damaged neuron [50] and theoretically could trigger DICTs, we performed cell-damaging experiments in homozygous CX3CR1GFP/GFP mice lacking the fractalkine receptor.