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. Author manuscript; available in PMC: 2014 Feb 3.
Published in final edited form as: Nat Med. 2013 Mar 24;19(4):473–480. doi: 10.1038/nm.3117

Figure 1. Neuropathology in the cortex and hippocampus of Snx27−/− mice.

Figure 1

(a) Expression pattern of Snx27, GluR1 and NR1 in the developmental mouse cerebrum. Brain lysates of C57Bl/6 mice at different postnatal days were analyzed by western blot to detect Snx27, GluR1, NR1 and β-actin (as loading control). Data represent mean ± s.e.m., n = 3.

(b) Decreased number and size of neurons in the cortex of Snx27−/− mice. Low (left panels) and high (right panels) magnification views of Nissl staining sections from Snx27+/+ (top panels) and Snx27−/− (bottom panels) mice (P14). Data represent mean ± s.e.m., n = 4. P values were calculated using two-tailed Student’s t test, *P < 0.05, **P < 0.01, ***P < 0.001. Bar=50μm.

(c,d) Decreased dendritic branches and lengths in cerebral cortex and hippocampus in Snx27−/− mice. Golgi staining of cortex (upper panels) and hippocampus (lower panels) of Snx27+/+ (left panels) and Snx27−/− (right panels) mice (P14) are presented in (c).

Quantitative analysis of apical and basal dendrites and total branch points in cortical layer 5 pyramidal and hippocampal neurons in Snx27+/+ and Snx27−/− mice are shown in (d). Data represent mean ± s.e.m., n = 4. P values were calculated using two-tailed Student’s t test, *P < 0.05, **P < 0.01, ***P < 0.001. Bar=100μm.