(A) Immunofluorescent staining of BrdU and Ki67 in the hypothalamus of WT (upper panels) and Hap1-null (KO, lower panels) mice that had been injected with BrdU at P1 for 2 hours. Scale bar: 10 μm. (B) Stereological quantification of the numbers of BrdU-positive cells in the brain regions of WT and Hap1-null mice (KO, left), and the ratio of these between KO and WT mice (right). n = 3 for each group, *P < 0.05. (C) Quantitative analysis of the number of BrdU-positive cells via stereology in Hap1 P1 KO and adult KO mice showing that loss of Hap1 only reduces neurogenesis in P1 KO mice. n = 3 for each genotype, *P < 0.05. (D) Western blots of the hypothalamic tissues of WT, heterozygous (Het), and homozygous (KO) Hap1-KO mice (P2) with antibodies to Hap1, Ki67, DCX, NeuN, GFAP, MBP, and Gapdh. Two different samples of each genotype are presented. (E) The ratios of proteins indicated in D to Gapdh were obtained from 3 independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001 compared with the KO sample. (F) Western blots of brain tissues of control, Hap1 P1 KO, and adult KO mice with antibodies to Hap1, Ki67, DCX, and Gapdh. Samples were analyzed after TM injection for 15 (P1 KO) or 30 (P1 and adult KO) days. (G) Relative levels of proteins (ratio to Gapdh) on the Western blots were presented. All error bars represent SEM.