Fig. 4From: Histamine induces microglia activation and dopaminergic neuronal toxicity via H1 receptor activationHistamine-induced ROS generation contributes to microglial phagocytosis. a Only 10 (H10) and 100 μM histamine (H100) significantly increased the levels of ROS as compared with untreated controls (Ctr). b Cellular ROS production induced by 100 μM histamine was blocked by an H1R antagonist (AntH1R, mepyramine maleate, 1 μM) or H4R antagonist (AntH4R, JNJ7777120, 5 μM) and mimicked by an H1R agonist (AgH1R, 4-methylhistamine dihydrochloride, 20 μM) or a H4R agonist (4-methylhistamine dihydrochloride, 20 μM). The involvement of other receptors was excluded since the application of their respective antagonists did not interfere with ROS levels induced by histamine (H2R antagonist (cimetidine), 5 μM; H3R antagonist (carcinine ditrifluoroacetate), 5 μM). Apocynin (5 μM) was used to rule out the involvement of the NADPH oxidase system in cellular production of ROS (c) and in the phagocytosis of IgG latex beads (d) induced by histamine. Apocynin-treated cells are represented in slashed columns both in (c and d). Data are expressed as mean ± SEM (n = 3–16) and as a percentage of control. *P < 0.05, **P < 0.01, and ***P < 0.001, using one-way ANOVA followed by Bonferroni’s multiple comparison testBack to article page