Cocaine-mediated induction of MCP-1 enhances monocyte transmigration both in vitro and in vivo. (A) Concentration-dependent transmigration of monocytes in the presence of CM from cocaine-treated BV-2 cells. (B) Increased monoctye transmigration in the presence of CM from cocaine-treated cells was ameliorated by the MCP-1–blocking antibody (1 μg/mL). (C) Pretreatment with BD1047 ameliorated cocaine-mediated increase in monoctye transmigration. (D) Pretreatment of monocytes with CCR2 antagonist RS102895 ameliorated cocaine-mediated increase in monoctye transmigration. All the data are presented as means ± SD of 4 individual experiments. *P < .05; **P < .01 versus control group; #P < .05 versus cocaine-treated group. (E) Detection of PKH26-labeled monocytes in the brains of mice treated with cocaine. Fluorescence micrographs show monocytes in the perivascular cuff (left panel; arrows) and the parenchymal (right panel; arrows) areas of the brain. (F) Increased monoctye transmigration observed in the cocaine-treated group was ameliorated by pretreatment of mice with BD1047. (G) Increased monocyte transmigration in the cocaine-treated WT but not CCR2 KO mice. *P < .05 versus saline group; #P < .05 versus cocaine group counted from the parenchyma. (F-G) Data are expressed as the mean number of PKH26-labeled cells in the entire area of 3 coronal brain sections ± SD (n = 6 per group).