Figure 7. Conditional ablation of microglia prevents the synaptic changes and the behavioral abnormalities resulting from SNI. A, The experimental diagram shows the timeline of drug treatments (TM, tamoxifen, DT, diphtheria toxin), immunostaining, Western blots (WB) pain behavioral tests (Pain beha.), novel object recognition test (NORT) and electrophysiology (EP) before and after SNI. B, The photographs show Iba1-positive microglia in the hippocampal CA1 area and spinal dorsal horn of CX3CR1CreER/+ (Control) and CX3CR1CreER/+: R26iDTR/+ mice (M-Abl) 3 d after SNI. C, Results of analyses of dendritic length (n = 12, basal, Control + Sham vs Control + SNI, p = 0.011, M-Abl + Sham vs M-Abl + SNI, p = 0.568; apical, Control + Sham vs Control + SNI, p = 0.035, M-Abl + Sham vs M-Abl + SNI, p = 0.399), branch number (n = 12, basal, Control + Sham vs Control + SNI, p = 0.013, M-Abl + Sham vs M-Abl + SNI, p = 0.208; apical, Control + Sham vs Control + SNI, p = 0.022, M-Abl + Sham vs M-Abl + SNI, p = 0.451), and spine densities of CA1 neurons in sham and SNI groups of control and M-Abl mice (n = 12, basal, Control + Sham vs Control + SNI, p = 0.039, M-Abl + Sham vs M-Abl + SNI, p = 0.602; apical, Control + Sham vs Control + SNI, p = 0.028, M-Abl + Sham vs M-Abl + SNI, p = 0.375; 12 neurons from 5 mice per group). D, The NMDA/AMPA current ratio at CA3-CA1 synapses in SNI group was lower in control mice but not in M-Abl mice, compared with sham groups (n = 14, Control + Sham vs Control + SNI, p = 0.022, M-Abl + Sham vs M-Abl + SNI, p = 0.412). E, Results of analyses of dendritic length (n = 12, Control + Sham vs Control + SNI, p = 0.021, M-Abl + Sham vs M-Abl + SNI, p = 0.226), branch number (n = 12, Control + Sham vs Control + SNI, p = 0.017, M-Abl + Sham vs M-Abl + SNI, p = 0.336), and spine densities of spinal NK1-PN neurons in sham and SNI groups of control and M-Abl mice (n = 12, Control + Sham vs Control + SNI, p = 0.014, M-Abl + Sham vs M-Abl + SNI, p = 0.433; 12 neurons from 5 mice per group). F, The NMDA/AMPA current ratio in spinal NK1-PNs in different groups (n = 12, Control + Sham vs Control + SNI, p = 0.031, M-Abl + Sham vs M-Abl + SNI, p = 0.522). 12 neurons from 5 mice per group. G, The recognition index for STM (n = 10, Control + Sham vs Control + SNI, p = 0.026, M-Abl + Sham vs M-Abl + SNI, p = 0.559) and mechanical allodynia (sample size mentioned in figure, day 3, Control + Sham vs Control + SNI, p < 0.001, M-Abl + Sham vs M-Abl + SNI, p = 0.306; day 5, Control + Sham vs Control + SNI, p < 0.001, M-Abl + Sham vs M-Abl + SNI, p = 0.528; day 7, Control + Sham vs Control + SNI, p < 0.001, M-Abl + Sham vs M-Abl + SNI, p = 0.672) in sham and SNI groups of control and M-Abl mice. H, The expression of TNF-α and BDNF in hippocampal (n = 5, TNF-α, Control + Sham vs Control + SNI, p < 0.001, M-Abl + Sham vs M-Abl + SNI, p = 0.162; BDNF, Control + Sham vs Control + SNI, p = 0.035, M-Abl + Sham vs M-Abl + SNI, p = 0.098) and spinal dorsal horn (n = 5, TNF-α, Control + Sham vs Control + SNI, p < 0.001, M-Abl + Sham vs M-Abl + SNI, p = 0.377; BDNF, Control + Sham vs Control + SNI, p < 0.001, M-Abl + Sham vs M-Abl + SNI, p = 0.568) tissues from the mice that had been used for the above behavioral tests. Values are the mean ± SEM *p < 0.05, **p < 0.01, ***p < 0.001 compared with the values for each of the other three groups. Data for graphs in G were analyzed using repeated-measures two-way ANOVA. Data for other graphs were analyzed using Student's t test.