Fig. 7

Hv1 is required for IFN-γ promotes neuropathic pain and astrocyte activation. A Mechanical allodynia in SNT mice treated with exogenous IFN-γ. IFN-γ (100U in 5 μl ACSF) was intrathecally applied at POD3 after SNT. Data are presented as mean ± SEM, n = 7 for control groups, n = 6 for IFN-γ treated group. ^#p < 0.05, Hv1 KO + saline vs Hv1 KO + IFN-γ, *p < 0.05, WT + saline vs. Hv1 KO + IFN-γ, unpaired t-test. B Mechanical allodynia in naïve mice treated with exogenous IFN-γ. IFN-γ (100U in 5 μl ACSF) was intrathecally applied after the baseline pain test. Data are presented as mean ± SEM, n = 6 mice for each group. **p < 0.01, ***p < 0.001. WT vs. Hv1 KO, unpaired t-test. C Representative images of Iba1 (top panels), GFAP (middle panels) and merged (bottom panels) immunoreactivity in the dorsal horn in control (a naïve WT sample was shown, left), IFN-γ–treated WT (center) IFN-γ–treated Hv1 KO (right) mice at day 4 post injection. Scale bar: 50 µm. D, E, Quantification of microglia (D) and astrocyte (E) density at POD4 in Hv1 WT and KO mice following IFN-γ treatment. Data are presented as mean ± SEM, n = 6 slices from 3 mice for each group. **p < 0.01. WT vs. Hv1 KO, unpaired t-test