Figure 1: Mechanisms underlying microglial response to peripheral inflammation. (A) Schematic representation of the signaling pathway underlying changes in microglial Ca2+ signaling, induced by peripheral inflammation. (B) Molecular mechanisms involved into the interplay between the increase in [Ca2+]i and the activation of the NLRP3 inflammasome. The boxed structure consisting of NLRP3, adaptor protein ASC and Pro-Caspase-1 represents the NLRP3 inflammasome. ADPR: ADP-ribose; ER: endoplasmic reticulum; IL: interleukin; IL-1R: IL-1β receptor; IP3: inositol 1,4,5-trisphosphate; MT: mitochondrion; mtDNA: mitochondrial DNA; mtROS: reactive oxygen species of mitochondrial origin; NF-κB: nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells; NLRP3: NACHT-, LRR- and pyrin (PYD)-domain-containing protein 3; P2X7: ionotropic ATP receptor; P2Y1, 2, 4, 6: metabotropic ATP receptors; PLC: phospholipase C; SOCE: store-operated Ca2+ entry channel; TNF-R: tumor necrosis factor-α receptor; TRPM2: transient receptor potential cation channel, subfamily M, member 2.