Fig. 1

CRPS-I mouse model showed persistent mechanical allodynia, accompanied with CXCL13 upregulation in ipsilateral spinal cord dorsal horn. A Protocol for the experiments. B 50% paw withdrawal threshold (PWT) measured in ipsilateral hindpaw before and after CPIP model establishment. C qPCR of Cxcl13 gene expression in ipsilateral SCDH of sham and CPIP model mice on Day 7. D Immunostaining showing CXCL13 expression in ipsilateral SCDH of CPIP mice on Day 14. Right panel: summary of normalized fluorescence intensity of CXCL13. Values were normalized with sham group. E Western blot showing CXCL13 expression in sham (left panel) and CPIP model group (right panel) on Day 0, 7 and 14. The upper panels show representative immunoblot images and the lower panels show pooled data. n = 5–6 mice/group. F–H Double immunostainings of CXCL13 with NeuN (neuron marker, F), GFAP (astrocyte marker, G) and Iba-1 (microglia marker, H). Quantification of cellular distribution was shown on the right (pooled from 4 to 5 mice/group). Scale bar indicates 50 μm. Two-way ANOVA with repeated measures followed with Tukey post hoc test was used for comparisons in A. Student’s t test was used for comparisons in C, D. One-way ANOVA followed with Tukey post hoc test was used for comparisons in E. **p < 0.01 vs. sham or CPIP D0 group