Figure 3
From: Developmental and oncogenic effects of Insulin-like Growth Factor-I in Ptc1+/- mouse cerebellum
Delayed differentiation in neural precursors caused by IGF-I altered expression. (A) Morphologic analysis of H&E-stained sagittal sections of mouse cerebellum at P15, showing physiological absence of EGL in the cerebellum of Ptc1+/+ mice. A thin 1-cell layer of EGL was present in the cerebellum of Ptc1+/+/IGF-I Tg (B), and Ptc1+/-mice (C). (D) A thicker 2-3-cells layer was observed in the EGL of Ptc1+/-/IGF-I Tg mice. (E) Western blot analysis showing the level of NeuN (48 and 46 kDa, solid and open square, respectively) expression in cerebellum from Ptc1+/+, Ptc1+/+/IGF-I Tg, Ptc1+/-, and Ptc1+/-/IGF-I Tg mice at P5, with relative β-actin to control protein loading. (F) Graphic representation of densitometric analysis. (G and H) Immunohistochemical analysis showing a decrease in the expression of NeuN in the IGL of the cerebellum of Ptc1+/-/IGF-I Tg mice (H) compared to Ptc1+/-mice (G). (I) Frequency of NeuN positive neurons in the IGL of Ptc1+/-and Ptc1+/-/IGF-I Tg mice. More than 5 × 103 granule neurons from 12 randomly selected digital images of the IGL (2 mice per genotype) have been examined.