Fig. 2: High dose diphtheria toxin non-specifically induced microglia activation.

a Representative Iba1 staining images from cortex. The enlarged images were from the areas indicated by the square frame of each group. b Cortical Iba1+ microglial cell densities showed that low dose DT (n = 16) treatment did not alter microglia density in the WT mice, but high dose (n = 19) significantly increased the density compared with no DT WT control (n = 12); Repopulated microglia in the low dose DT (n = 14) treated DTR mice reached basal cell density (n = 12) at 10 days, but was significantly increased in the high dose DT (n = 18) group. The microglia depletion efficiencies between the high (n = 8) and lose dose (n = 10) DT groups were comparable. (****p < 0.0001, t-test, two sides). c Soma size measurement showed dramatic cell body enlargement in the high dose (n = 36) but not low dose DT (n = 36) treated WT mice, and in the high dose (n = 36) but not low dose DT (n = 36) treated DTR mice (n = 36 for no DT WT, n = 33 for no DT DTR group, ****p < 0.0001, *p = 0.0129, t-test, two sides). d Sholl analysis of individual Iba1+ microglia cells showed that the low dose DT (n = 13) treatment in WT mice did not alter microglia morphology compared with no DT controls (n = 17, WT and DTR control data were pooled together, p = 0.9837). Microglia from both high dose DT treated WT (n = 17) and DTR (n = 16) mice showed similar less interactions than no DT controls (p < 0.0001). Microglia from the low dose DT treated DTR (n = 14) mice also showed less interactions than no DT controls (p < 0.0001) Two-way ANOVA with repeated measurement (b–d, images collected from 3 mice for each group, except n = 5 mice for the low dose DT ablation at 2 days). Data were presented as mean ± SEM. Source data are provided as a Source Data file for (b–d).