Figure 4. RIIβ re-expression in the hypothalamus reverses the prolonged leptin-induced pSTAT3 signalling.

(a) Representative images (two or more sections from two to three mice) of CreGFP fluorescence and pSTAT3 immunofluorescent staining in the ventral hypothalamus from RIIβ^lox/lox mice injected with AAV1-CreGFP unilaterally and 4 h following leptin i.p. injection (1 mg kg⁻¹). Both CreGFP and pSTAT3 were localized to cell nucleus. 3V, third ventricle; ARC, arcuate nucleus; VMH, ventromedial hypothalamic nucleus. Scale bars, 200 μm. (b) Quantification of pSTAT3-positive cells in the ARC side with AAV-CreGFP infection and in the saline-injected control side from mice 1 and 4 h following leptin i.p. injection (1 mg kg⁻¹). Multiple sections from two mice (1 h) and three mice (4 h) were counted and averaged, and presented as cells per section. (c) Representative images of RIIβ and pSTAT3 immunofluroscent staining in the hypothalamus from RIIβ^Vgat mice 1 and 4 h following leptin i.p. injection (1 mg kg⁻¹). Scale bars, 200 μm. (d) Quantification of pSTAT3-positive cells in hypothalamic regions ARC, VMH, DMH and lateral hypothalamus (LH) from RIIβ^Vgat mice 1 and 4 h following leptin i.p. injection as shown in c and Supplementary Fig. 1e. Sections from three mice per group were counted and averaged and presented as cells per section. Data were presented as mean±s.e.m. and analysed by two-tail Student's t-test (*P<0.05, ***P<0.001).