Figure 4

Correlation between enhancement of adult neurogenesis and dematuration of GCs. (A) Representative images of calbindin-IR. GCL: granule cell layer, ML: molecular layer. Scale bar: 100 μm. (B) Quantification of calbindin-IR in the GCL and the ML in WT mice and 5-HT4R KO mice. Data are expressed as the mean ± SEM (n = 4 or 5). Main effect of drug: P = 0.0014 (GCL), P = 0.0015 (ML); main effect of genotype: P = 0.0237 (GCL), P = 0.0208 (ML); interaction of drug and genotype: P = 0.0022 (GCL), P = 0.0009 (ML); P values determined by two-way ANOVA. *** P < 0.001 and N.S., not significant for post hoc Bonferroni’s test, respectively, after two-way ANOVA. (C) Comparison between the number of BrdU-positive cells in the SGZ and calbindin-IR intensity of the granule cell layer in WT mice. Mice that received fluoxetine treatment (22 mg/kg) for 3 or 4 weeks were plotted in the analysis. The Pearson correlation coefficient (R) was calculated (P = 0.0278). (D) Comparison of gene expression changes after chronic fluoxetine treatment between calbindin (Calb1) and Bdnf or Npy. Gene expression was normalized by the average gene expression in control mice. Mice received fluoxetine treatment (22 mg/kg) for 3 or 4 weeks. Four independent experiments were included in the analysis. The Pearson correlation coefficient (R) was calculated (Bdnf vs. Calb1, P = 0.0002, Npy vs. Calb1, P < 0.0001).