FIGURE 3.

Minocycline treatment ameliorates IFN-α-induced neurogenic defects and depressive behaviors. (A) Experimental design. (B–E) Quantification of proliferating cells in the SGZ following the 4-week treatment with PBS or IFN-α, in the absence or presence of minocycline (Mino). The brain sections were immunostained for the proliferation marker, Ki67 (B) and neuronal progenitor marker, TBR2 (C), and then the Ki67+ and TBR2+ cells in the SGZ were counted and compared among the treatment groups (Ki67, D; TBR2, E). n = 7 mice per group. (F,G) Quantification of newly generated neurons in the DG after the 5-week IFN-α treatment. The new neurons were labeled with BrdU administered at the beginning at the 5th week of the IFN-α treatment and visualized by immunostaining for BrdU and DCX, a marker of immature neurons (F) The number of BrdU⁺DCX⁺ cells in the DG was counted and compared among the groups. n = 5 mice per group. (H,I) The effects of IFN-α and minocycline on depression-like behaviors in mice. After the final injection of IFN-α and/or minocycline, the mice were subjected to the tail suspension (H) and forced swimming test (I). The immobility times observed in these tests were quantified and compared among the groups. n = 10 mice per group. *P < 0.05; **P < 0.01; Error bars: means ± SEM; Scale bars: (B,C) = 100 μm; (F) = 25 μm.