[1] K. D. Rochfort and P. M. Cummins, “The blood-brain barrier endothelium: a target for pro-inflammatory cytokines.,” Biochemical Society transactions, vol. 43, no. 4, pp. 702–706, Aug. 2015.
[2] H. O. Kalkman and D. Feuerbach, “Antidepressant therapies inhibit inflammation and microglial M1-polarization.,” Pharmacology & therapeutics, vol. 163, pp. 82–93, Jul. 2016.
[3] H. J. Park, S. H. Oh, H. N. Kim, Y. J. Jung, and P. H. Lee, “Mesenchymal stem cells enhance α-synuclein clearance via M2 microglia polarization in experimental and human parkinsonian disorder.,” Acta neuropathologica, vol. 132, no. 5, pp. 685–701, Nov. 2016.
[4] P. Illes, P. Rubini, H. Ulrich, Y. Zhao, and Y. Tang, “Regulation of Microglial Functions by Purinergic Mechanisms in the Healthy and Diseased CNS.,” Cells, vol. 9, no. 5, p 1108, Apr. 2020.
[5] M. K. Zabel and W. M. Kirsch, “From development to dysfunction: microglia and the complement cascade in CNS homeostasis.,” Ageing research reviews, vol. 12, no. 3, pp. 749–756, Jun. 2013.
[6] T. Rőszer, “Understanding the Mysterious M2 Macrophage through Activation Markers and Effector Mechanisms.,” Mediators of inflammation, vol. 2015, p. 816460, 2015.
[7] H. Hirbec, F. Rassendren, and E. Audinat, “Microglia Reactivity: Heterogeneous Pathological Phenotypes.,” Methods in molecular biology (Clifton, N.J.), vol. 2034, pp. 41–55, 2019.
[8] S. A. Liddelow and B. A. Barres, “Reactive Astrocytes: Production, Function, and Therapeutic Potential.,” Immunity, vol. 46, no. 6, pp. 957–967, Jun. 2017.
[9] J. A. Orellana et al., “Amyloid β-induced death in neurons involves glial and neuronal hemichannels.,” The Journal of neuroscience : the official journal of the Society for Neuroscience, vol. 31, no. 13, pp. 4962–4977, Mar. 2011.
[10] J. A. Orellana et al., “ATP and glutamate released via astroglial connexin 43 hemichannels mediate neuronal death through activation of pannexin 1 hemichannels.,” Journal of neurochemistry, vol. 118, no. 5, pp. 826–840, Sep. 2011.
[11] B. Sperlágh and P. Illes, “Purinergic modulation of microglial cell activation.,” Purinergic signalling, vol. 3, no. 1–2, pp. 117–127, Mar. 2007.
[12] R. J. Rodrigues, A. R. Tomé, and R. A. Cunha, “ATP as a multi-target danger signal in the brain.,” Frontiers in neuroscience, vol. 9, p. 148, 2015.
[13] S. E. Haynes et al., “The P2Y12 receptor regulates microglial activation by extracellular nucleotides.,” Nature neuroscience, vol. 9, no. 12, pp. 1512–1519, Dec. 2006.
[14] L.-P. Bernier, A. R. Ase, É. Boué-Grabot, and P. Séguéla, “Inhibition of P2X4 function by P2Y6 UDP receptors in microglia.,” Glia, vol. 61, no. 12, pp. 2038–2049, Dec. 2013.
[15] H. Franke, A. Verkhratsky, G. Burnstock, and P. Illes, “Pathophysiology of astroglial purinergic signalling.,” Purinergic signalling, vol. 8, no. 3, pp. 629–657, Sep. 2012.
[16] G. Haskó and B. Cronstein, “Regulation of inflammation by adenosine.,” Frontiers in immunology, vol. 4, p. 85, 2013.
[17] N. Nedeljkovic, “Complex regulation of ecto-5’-nucleotidase/CD73 and A(2A)R-mediated adenosine signaling at neurovascular unit: A link between acute and chronic neuroinflammation.,” Pharmacological research, vol. 144, pp. 99–115, Jun. 2019.
[18] H. Zimmermann, M. Zebisch, and N. Sträter, “Cellular function and molecular structure of ecto-nucleotidases.,” Purinergic signalling, vol. 8, no. 3, pp. 437–502, Sep. 2012.
[19] M. Matyash, O. Zabiegalov, S. Wendt, V. Matyash, and H. Kettenmann, “The adenosine generating enzymes CD39/CD73 control microglial processes ramification in the mouse brain.,” PloS one, vol. 12, no. 4, p. e0175012, 2017.
[20] I. Grković, D. Drakulić, J. Martinović, and N. Mitrović, “Role of Ectonucleotidases in Synapse Formation During Brain Development: Physiological and Pathological Implications.,” Current neuropharmacology, vol. 17, no. 1, pp. 84–98, 2019.
[21] I. Grković, N. Mitrović, M. Dragić, M. Adžić, D. Drakulić, and N. Nedeljković, “Spatial Distribution and Expression of Ectonucleotidases in Rat Hippocampus After Removal of Ovaries and Estradiol Replacement,” Molecular Neurobiology, vol. 56, no. 3, pp 1933-1945, Jul. 2019.
[22] G. Burnstock, “Purinergic Signalling: Therapeutic Developments.,” Frontiers in pharmacology, vol. 8, p. 661, 2017.
[23] L. Antonioli, P. Pacher, E. S. Vizi, and G. Haskó, “CD39 and CD73 in immunity and inflammation.,” Trends in molecular medicine, vol. 19, no. 6, pp. 355–367, Jun. 2013.
[24] M. C. Geloso, V. Corvino, and F. Michetti, “Trimethyltin-induced hippocampal degeneration as a tool to investigate neurodegenerative processes.,” Neurochemistry international, vol. 58, no. 7, pp. 729–738, Jun. 2011.
[25] A. Trabucco et al., “Methylated tin toxicity a reappraisal using rodents models.,” Archives italiennes de biologie, vol. 147, no. 4, pp. 141–153, Dec. 2009.
[26] V. Corvino et al., “Estrogen administration modulates hippocampal GABAergic subpopulations in the hippocampus of trimethyltin-treated rats.,” Frontiers in cellular neuroscience, vol. 9, p. 433, 2015.
[27] W. Lattanzi, V. Corvino, V. Di Maria, F. Michetti, and M. C. Geloso, “Gene expression profiling as a tool to investigate the molecular machinery activated during hippocampal neurodegeneration induced by trimethyltin (TMT) administration.,” International journal of molecular sciences, vol. 14, no. 8, pp. 16817–16835, Aug. 2013.
[28] M. Dragić, M. Zarić, N. Mitrović, N. Nedeljković, and I. Grković, “Two Distinct Hippocampal Astrocyte Morphotypes Reveal Subfield-Different Fate during Neurodegeneration Induced by Trimethyltin Intoxication.,” Neuroscience, vol. 423, pp. 38–54, Dec. 2019.
[29] L. Latini et al., “Trimethyltin intoxication up-regulates nitric oxide synthase in neurons and purinergic ionotropic receptor 2 in astrocytes in the hippocampus.,” Journal of neuroscience research, vol. 88, no. 3, pp. 500–509, Feb. 2010.
[30] S. Haga, C. Haga, T. Aizawa, and K. Ikeda, “Neuronal degeneration and glial cell-responses following trimethyltin intoxication in the rat.,” Acta neuropathologica, vol. 103, no. 6, pp. 575–582, Jun. 2002.
[31] A. R. Little, D. B. Miller, S. Li, M. L. Kashon, and J. P. O’Callaghan, “Trimethyltin-induced neurotoxicity: gene expression pathway analysis, q-RT-PCR and immunoblotting reveal early effects associated with hippocampal damage and gliosis.,” Neurotoxicology and teratology, vol. 34, no. 1, pp. 72–82, 2012.
[32] N. Mitrović et al., “Regional and sex-related differences in modulating effects of female sex steroids on ecto-5’-nucleotidase expression in the rat cerebral cortex and hippocampus.,” General and comparative endocrinology, vol. 235, pp. 100–107, Sep. 2016.
[33] N. Mitrović et al., “17β-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes.,” Journal of molecular neuroscience : MN, vol. 61, no. 3, pp. 412–422, Mar. 2017.
[34] M. Dragić, M. Zarić, N. Mitrović, N. Nedeljković, and I. Grković, “Application of Gray Level Co-Occurrence Matrix Analysis as a New Method for Enzyme Histochemistry Quantification,” Microscopy and Microanalysis, 2019.
[35] K. W. Dunn, M. M. Kamocka, and J. H. McDonald, “A practical guide to evaluating colocalization in biological microscopy.,” American journal of physiology. Cell physiology, vol. 300, no. 4, pp. C723-42, Apr. 2011.
[36] S. Tsutsumi, M. Akaike, H. Arimitsu, H. Imai, and N. Kato, “Circulating corticosterone alters the rate of neuropathological and behavioral changes induced by trimethyltin in rats.,” Experimental neurology, vol. 173, no. 1, pp. 86–94, Jan. 2002.
[37] F. Jauregui-Huerta, Y. Ruvalcaba-Delgadillo, R. Gonzalez-Castañeda, J. Garcia-Estrada, O. Gonzalez-Perez, and S. Luquin, “Responses of glial cells to stress and glucocorticoids.,” Current immunology reviews, vol. 6, no. 3, pp. 195–204, Aug. 2010.
[38] B. S. Carter, D. E. Hamilton, and R. C. Thompson, “Acute and chronic glucocorticoid treatments regulate astrocyte-enriched mRNAs in multiple brain regions in vivo.,” Frontiers in neuroscience, vol. 7, p. 139, 2013.
[39] C. D. Balaban, J. P. O’Callaghan, and M. L. Billingsley, “Trimethyltin-induced neuronal damage in the rat brain: comparative studies using silver degeneration stains, immunocytochemistry and immunoassay for neuronotypic and gliotypic proteins.,” Neuroscience, vol. 26, no. 1, pp. 337–361, Jul. 1988.
[40] A. Verkhratsky, J. J. Rodrigues, A. Pivoriunas, R. Zorec, and A. Semyanov, “Astroglial atrophy in Alzheimer’s disease.,” Pflugers Archiv : European journal of physiology, vol. 471, no. 10, pp. 1247–1261, Oct. 2019.
[41] L. Erb, L. T. Woods, M. G. Khalafalla, and G. A. Weisman, “Purinergic signaling in Alzheimer’s disease.,” Brain research bulletin, vol. 151, pp. 25–37, Sep. 2019.
[42] M. Cieślak and A. Wojtczak, “Role of purinergic receptors in the Alzheimer’s disease.,” Purinergic signalling, vol. 14, no. 4, pp. 331–344, Dec. 2018.
[43] N. Braun et al., “Assignment of ecto-nucleoside triphosphate diphosphohydrolase-1/cd39 expression to microglia and vasculature of the brain.,” The European journal of neuroscience, vol. 12, no. 12, pp. 4357–4366, Dec. 2000.
[44] F. Hao et al., “Chemokine fractalkine attenuates overactivation and apoptosis of BV-2 microglial cells induced by extracellular ATP.,” Neurochemical research, vol. 38, no. 5, pp. 1002–1012, May 2013.
[45] F. L. Heppner, K. Roth, R. Nitsch, and N. P. Hailer, “Vitamin E induces ramification and downregulation of adhesion molecules in cultured microglial cells.,” Glia, vol. 22, no. 2, pp. 180–188, Feb. 1998.
[46] M. A. Wollmer, R. Lucius, H. Wilms, J. Held-Feindt, J. Sievers, and R. Mentlein, “ATP and adenosine induce ramification of microglia in vitro.,” Journal of neuroimmunology, vol. 115, no. 1–2, pp. 19–27, Apr. 2001.
[47] D. Boche, V. H. Perry, and J. A. R. Nicoll, “Review: activation patterns of microglia and their identification in the human brain.,” Neuropathology and applied neurobiology, vol. 39, no. 1, pp. 3–18, Feb. 2013.
[48] W. Y. Tam and C. H. E. Ma, “Bipolar/rod-shaped microglia are proliferating microglia with distinct M1/M2 phenotypes.,” Scientific reports, vol. 4, p. 7279, Dec. 2014.
[49] A. G. Orr, A. L. Orr, X.-J. Li, R. E. Gross, and S. F. Traynelis, “Adenosine A(2A) receptor mediates microglial process retraction.,” Nature neuroscience, vol. 12, no. 7, pp. 872–878, Jul. 2009.
[50] K. Ohsawa, T. Sanagi, Y. Nakamura, E. Suzuki, K. Inoue, and S. Kohsaka, “Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration.,” Journal of neurochemistry, vol. 121, no. 2, pp. 217–227, Apr. 2012.
[51] S. Koizumi et al., “UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis.,” Nature, vol. 446, no. 7139, pp. 1091–1095, Apr. 2007.
[52] M. Adzic and N. Nedeljkovic, “Unveiling the Role of Ecto-5’-Nucleotidase/CD73 in Astrocyte Migration by Using Pharmacological Tools.,” Frontiers in pharmacology, vol. 9, p. 153, 2018.
[53] C. J. Ferrante et al., “The adenosine-dependent angiogenic switch of macrophages to an M2-like phenotype is independent of interleukin-4 receptor alpha (IL-4Rα) signaling.,” Inflammation, vol. 36, no. 4, pp. 921–931, Aug. 2013.
[54] M. Jakovljevic et al., “Induction of NTPDase1/CD39 by Reactive Microglia and Macrophages Is Associated With the Functional State During EAE.,” Frontiers in neuroscience, vol. 13, p. 410, 2019.
[55] M. Ramanathan et al., “Differential regulation of HIF-1alpha isoforms in murine macrophages by TLR4 and adenosine A(2A) receptor agonists.,” Journal of leukocyte biology, vol. 86, no. 3, pp. 681–689, Sep. 2009.
[56] G. Pinhal-Enfield et al., “An angiogenic switch in macrophages involving synergy between Toll-like receptors 2, 4, 7, and 9 and adenosine A(2A) receptors.,” The American journal of pathology, vol. 163, no. 2, pp. 711–721, Aug. 2003.
[57] F. Di Virgilio, “Liaisons dangereuses: P2X(7) and the inflammasome.,” Trends in pharmacological sciences, vol. 28, no. 9, pp. 465–472, Sep. 2007.
[58] S. Viana da Silva et al., “Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors.,” Nature communications, vol. 7, p. 11915, Jun. 2016.
[59] E. Faivre et al., “Beneficial Effect of a Selective Adenosine A(2A) Receptor Antagonist in the APPswe/PS1dE9 Mouse Model of Alzheimer’s Disease.,” Frontiers in molecular neuroscience, vol. 11, p. 235, 2018.
[60] A. Delekate, M. Füchtemeier, T. Schumacher, C. Ulbrich, M. Foddis, and G. C. Petzold, “Metabotropic P2Y1 receptor signalling mediates astrocytic hyperactivity in vivo in an Alzheimer’s disease mouse model.,” Nature communications, vol. 5, p. 5422, Nov. 2014.
[61] N. Reichenbach et al., “P2Y1 receptor blockade normalizes network dysfunction and cognition in an Alzheimer’s disease model.,” The Journal of experimental medicine, vol. 215, no. 6, pp. 1649–1663, Jun. 2018.
[62] D. O. Borroto-Escuela, S. Hinz, G. Navarro, R. Franco, C. E. Müller, and K. Fuxe, “Understanding the Role of Adenosine A2AR Heteroreceptor Complexes in Neurodegeneration and Neuroinflammation.,” Frontiers in neuroscience, vol. 12, p. 43, 2018.