Caspase 3 inhibitor prevents the KA-promoted hippocampal neurogenesis and microglial activation, but not astrogliosis, in the KA-icv-injected mice. CD-1 mice received KA-icv-injections and were sacrificed at day 1 to 7 post KA-injection. For control, the mice were sacrificed at day 7 post vehicle-injection (veh). (a and b) The neurogenesis and astrogliosis in the ipsilateral side of DG was examined by anti-DCX (red) and anti-GFAP (green) antibodies. Cell nuclei were stained with Hoechst 33258 (blue). Panel (a) shows the representative GFAP and DCX fluorescent images of DG at day 7 post KA-injection as compared with vehicle injection. Panel (b) shows the calculated number of DCX-positive neurons in 250 μm × 250 μm field. The data are represented as the percentage related to the control (veh). (c and d) CD-1 mice received KA-icv-injections alone (KA-7d) or co-injection of KA with caspase 3 inhibitor (KA + Cas3I-7d) or vehicle (veh), and were sacrificed at day 7 post KA-injection. The neurogenesis, microglial activation and astrogliosis in the suprapyramidal blade of DG was examined by anti-DCX (red), anti-GFAP (green) and anti-Iba-1 (blue) antibodies, respectively. Panel (c) shows the representative fluorescent images of GFAP, DCX and Iba-1 of DG at day 7 post KA-injection as compared with vehicle injection. The dotted lines define the molecular layer (ML), granular layer (GL) and subgranular zone (SGZ) of DG. Panel (d) shows the calculated number of DCX-positive neurons in the 250 μm × 250 μm field. The results are the mean ± S.D. from 8 images. Significant differences between the control (veh) and the KA injection are indicated by ***, P < 0.001. Significant differences between the KA injection alone and the co-injection of KA and caspase 3 inhibitor are indicated by ###, P < 0.001.