(A) Immunostaining of the hypothalamus of Hap1 P1 KO mouse with antibodies to NeuN and NPYY1R. Scale bar: 10 μm. (B) Quantitative analysis (n = 15 images per group) of the numbers (% of total cells) of NPYY1R-positive cells in WT, P1 KO, and adult KO (see Supplemental Figure 6) mouse hypothalamus (upper panel) and the stereology analysis of the numbers of NeuN-positive cells in Hap1 P1 KO and WT mouse hypothalamus (lower panel, n = 3 per genotype). (C) Western blot analysis of the hypothalamic tissues of WT and Hap1 P1 KO mice and quantifications. (D) Western blot analysis (left panel) and quantification (middle panel) of WT and Hap1-null (KO) mouse hypothalamic tissues showing decreased TrkB and its signaling (pTrkB, pAkt) when Hap1 is absent. The ratios of pTrkB to TrkB and pAkt to Akt between WT and KO mice were also shown (right panel). *P < 0.05. (E) Western blot of hypothalamic tissues from WT P1 mice that were injected into the third ventricle with either control (sterile PBS) for 2 hours, or 5 μg BDNF for 1 or 2 hours. Noninjected littermate served as control. (F) BrdU immunostaining of hypothalamus from P1 WT and Hap1-null (KO) mice that had been injected with either control or BDNF for 4 hours. Scale bar: 10 μm. (G) Quantification of BrdU-positive cells in the hypothalamus of control or BDNF-treated P1 WT or KO mice (n = 3 mice per genotype). **P < 0.01. All error bars represent SEM.