Fig. 3.

Effects of acute and chronic stress on hippocampal neurogenesis (cell proliferation) and sucrose consumption in IL-1RI null mice. (A–C) Acute stress (aSTR, immobilization and rotation, 50 min) decreased the number of BrdU⁺ cells in the DG of WT (A) but not IL-1RI null mice (KO, B) (main effect aSTR: F_1,31 = 8.297, P < 0.01; main effect genotype: F_1,31 = 6.874, P < 0.05; aSTR × genotype: F_1,31 = 1.559, P = n.s.; n = 8 per group). Note that the number of BrdU⁺ cells was not significantly different between nonstressed (Non-aSTR) WT and KO mice, indicating no difference in the baseline effect of IL-1RI null mutation. (D) Four-week CUS also significantly decreased the BrdU⁺ cell numbers in WT mice but not in IL-1RI KO mice (F_1,22 = 1.933, P = n.s.; n = 5–6 per group). CUS KO mice showed more BrdU⁺ cells than CUS WT mice. There was also no difference in baseline. (E) CUS also decreased the number of immature neurons, determined by colabeling of BrdU with DCX, and this effect was blocked in the IL-1RI KO mice. (F) In the sucrose consumption test, there was no baseline difference between WT and IL-1RI KO mice. CUS significantly decreased sucrose consumption in WT but not in IL-1RI KO mice (main effect CUS: F_1,22 = 1.361, P = n.s.; main effect genotype: F_1,22 = 5.191, P < 0.05; CUS × genotype: F_1,22 = 11.388, P < 0.01). (G) There was no difference in water consumption among groups (main effect CUS: F_1,22 = 0.305, P = n.s.; main effect genotype: F_1,22 = 0.040, P = n.s.; CUS × genotype: F_1,22 = 0.006, P = n.s.). (H) Experimental procedures for CUS in mice. CUS mice were exposed to two or three stressors per day for 28 days and received BrdU daily for 4 days of the last CUS period. On the last CUS day, sucrose consumption test (SCT) was conducted. Mice were killed 14 days after last BrdU administration. **, P < 0.01 compared with nonstressed WT mice; #, P < 0.05, ##, P < 0.01 compared with stressed WT mice in the Tukey's post hoc test, mean ± SEM.