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. 2018 May 22;11:1756286418774254. doi: 10.1177/1756286418774254

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© The Author(s), 2018

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 3. — Nucleotide-associated pathways in microglia. A toll-like receptor (TLR) agonist such as lipopolysaccharide (LPS) leads to the release of proinflammatory mediators such as interleukin (IL)-6 in an ATP-dependent manner. Signaling through P2X4 receptors enhances migration of microglia. Uridine triphosphate (UTP) binds to P2Y2/4, Uridine diphosphate (UDP) to P2Y6 and adenosine diphosphate (ADP) to P2Y12, which results in a higher rate of phagocytosis. 2’,3’-cyclic adenosine monophosphate (cAMP) is released from damaged cells and is metabolized by an extracellular pathway to 2’- and 3’-adenosine monophosphate (AMP), which is then metabolized to adenosine. After adenosine has activated its A1 receptor, it possesses neuroprotective functions.