Fig. 4From: CXCL13 contributes to chronic pain of a mouse model of CRPS-I via CXCR5-mediated NF-κB activation and pro-inflammatory cytokine production in spinal cord dorsal hornCXCR5 is essential for mediating mechanical/cold allodynia as well as c-Fos and glial cell overactivation in ipsilateral SCDH of CPIP mice. A Time course showing 50% PWT changes in ipsilateral hindpaws of WT and Cxcr5−/− mice after CPIP model establishment. B Summary of normalized AUC of curves in A. C Time course showing cold allodynia behaviors in ipsilateral hindpaws of WT and Cxcr5−/− mice upon acetone application. D Summary of normalized AUC of curves in C. E–G Immunostaining of GFAP (E), Iba-1 (F) and c-Fos (G) in ipsilateral SCDH from WT + sham, WT + CPIP, Cxcr5−/− + sham and Cxcr5−/− + CPIP groups. H–J Summary of GFAP (H) & Iba-1 (I) fluorescence intensity and c-Fos (J) positively stained cell number. n = 5–6 mice/group. *p < 0.05, **p < 0.01 vs. WT + sham group; #p < 0.05, ##p < 0.01 vs. WT + CPIP group. Scale bar indicates 50 μm. Two-way ANOVA with repeated measures followed by Tukey’s post hoc test was used for comparisons in A, C. One-way ANOVA followed by Tukey’s post hoc test was used for comparisons in othersBack to article page