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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Physiol Behav. 2016 Sep 1;167:16–27. doi: 10.1016/j.physbeh.2016.08.036

Fig. 2.

Fig. 2

The 5-AzaC treatment of P7 mice induces neurodegeneration. (A) Western blot analysis of CC3 HP, NC and CB in cytosolic extracts from the saline- and 5-AzaC-treated (0–10 mg/kg, s. c. 8 h) groups. (B) Western blot analysis of CC3 using cytosolic extracts of the HP and NC from the saline- and 5-AzaC-treated (5 mg/kg, s. c.) groups at various time points. Ponceau S staining confirmed equal loading of the protein, and β-actin was used as a loading controls Error bars, SEM (n = 10 pups/group). (C) Free-floating coronal brain sections (hippocampus and retrosplenial cortex) from the saline- and 5-AzaC-treated (5 mg/kg, s. c. 8 h) animals were immunostained with an anti-rabbit CC3 antibody. The white arrows indicate the CC3-positive neurons in the hippocampus and retrosplenial cortex. Scale bars = 200 μm. The hippocampal region was enlarged to show the CC3-positive cells (*). The scale bars represent 50 μm. The CC3-positive cells in the hippocampus and retrosplenial cortex were counted. Error bars, SEM (n = 5 pups/group). *p < 0.01 vs. 0 h (saline).