2016
DOI: 10.1016/j.neuropharm.2015.08.005
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Purinergic neurone-glia signalling in cognitive-related pathologies

Abstract: Neuroglia, represented by astrocytes, oligodendrocytes, NG glia and microglia are homeostatic, myelinating and defensive cells of the brain. Neuroglial cells express various combinations of purinoceptors, which contribute to multiple intercellular signalling pathways in the healthy and diseased nervous system. Neurological diseases are invariably associated with profound neuroglial remodelling, which is manifest by reactive gliosis, pathological remodelling and functional atrophy of various types of glial cell… Show more

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Cited by 30 publications
(17 citation statements)
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References 224 publications
(142 reference statements)
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“…We found that the surface expression of P2X7Rs was robust in CD206 High MHCII Low macrophages, but very low in microglia, in both WT and Mecp2 308/Y mice (other myeloid subsets expressed intermediate levels). This finding seems to be at odds with previous reports of high P2X7R expression in microglia in cognitive-related pathologies 32 . Such discrepancy can be attributed to minimal microglia activation in the cortex of Mecp2 308 mice, as well as our excluding macrophages in the flow cytometry analysis.…”
Section: Discussioncontrasting
confidence: 98%
See 1 more Smart Citation
“…We found that the surface expression of P2X7Rs was robust in CD206 High MHCII Low macrophages, but very low in microglia, in both WT and Mecp2 308/Y mice (other myeloid subsets expressed intermediate levels). This finding seems to be at odds with previous reports of high P2X7R expression in microglia in cognitive-related pathologies 32 . Such discrepancy can be attributed to minimal microglia activation in the cortex of Mecp2 308 mice, as well as our excluding macrophages in the flow cytometry analysis.…”
Section: Discussioncontrasting
confidence: 98%
“…Among leukocytes detected in the cortex, CD206 High MHCII Low macrophages had the most abundant surface P2X7R expression, while Ly6C High monocytes and CD206 Low MHCII High macrophages expressed intermediate levels. P2X7R expression in microglia has been documented in previous studies 17,32,33 . Interestingly, among all myeloid populations detected in the cortex, we found that microglia had the lowest levels of surface P2X7Rs (Fig.…”
Section: Resultsmentioning
confidence: 56%
“…In addition to these examples of neurodenerative illnesses, where glutamate/adenosine interaction is most prominent, secondary degeneration of neurons and glial cells in CNS trauma, ischemia, stroke, Alzheimer's disease, PD, HD, multiple sclerosis, amyotrophic lateral sclerosis and epilepsy occurs due to P2X7 receptor activation because of the massive release of ATP from the damaged brain or spinal cord tissue [202,329,330]. On the one hand, P2X7 receptors localized at the nerve terminals themselves or at astrocytes signalling to these terminals may greatly increase the release of glutamate, and on the other hand, P2X7 receptors can directly damage neurons and glial cells [331,332].…”
Section: Interplay Between Purinergic and Glutamatergic Systems In Thmentioning
confidence: 99%
“…All neurodegenerative illnesses are accompanied by cellular damage in the neighbourhood of the immediately afflicted area. This secondary degeneration may be prevented/ameliorated by P2X7 receptor antagonists [329]. In addition, multiple interactions of P2X7 receptors with postsynaptic glutamate effects have to be also considered.…”
Section: Interplay Between Purinergic and Glutamatergic Systems In Thmentioning
confidence: 99%
“…Gs/Gi protein activation, however, will work through the stimulation/inhibition of adenylate cyclase, respectively, with subsequent up-or down-regulation of cyclic AMP (cAMP) production. Final effects of purinergic receptor-promoted signaling will depend on the cell type and other intra-/intercellular conditions, as i.e., in physiological embryonic and adult neurogenesis (Oliveira et al, 2016), and in various pathological scenarios, such as inflammatory (Beamer et al, 2016;Madeira et al, 2017;Przybyła et al, 2018), oncological (Allard et al, 2016;Vijayan et al, 2017;Whiteside, 2017;Kazemi et al, 2018), neurological (Burnstock et al, 2011;Stockwell et al, 2017), metabolic (Lindberg et al, 2015;Csóka et al, 2017;Parpura et al, 2017;Tozzi and Novak, 2017;Labazi et al, 2018), psychiatric (Cunha, 2008;Lindberg et al, 2015;Ortiz et al, 2015;Krügel, 2016;Cheffer et al, 2017;Oliveros et al, 2017), cognitive (Illes and Verkhratsky, 2016), and peripheral neuromuscular and/or neuromotor diseases (Robitaille, 1995;Kalmar, 2005;Burnstock et al, 2013;Jiménez et al, 2014;Bogacheva and Balezina, 2015;Puchałowicz et al, 2015;Safarzadeh et al, 2016).…”
Section: Introductionmentioning
confidence: 99%