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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Int J Neuropsychopharmacol. 2011 Jul 22;15(8):1073–1086. doi: 10.1017/S1461145711001180

Fig 3.

Fig 3

Cysteamine treatment ameliorates the changes in BDNF expression in frontal cortex and hippocampus of heterozygous reeler mice (HRM). Cysteamine (150 mg/kg) or water (vehicle) was administered through drinking water to HRM and wild-type (WT) mice for 14 (Figs 3A and 3B) or 30 (Figs 3C and 3D) days. Mature BDNF (m-BDNF), truncated BDNF (trunc-BDNF) and pro-BDNF were determined by western blot analysis in frontal cortex (Figs 3A and 3C) and hippocampus (Figs 3B and 3D). WT-V: wild-type treated with vehicle (water); WT-C: wild-type treated with cysteamine; HRM-V: Heterozygous reeler mice treated with vehicle; HRM-C: Heterozygous reeler mice treated with cysteamine. Solid bars represent m-BDNF, open bars represent pro-BDNF and stripped bars represent trunc-BDNF. Data represent mean±SE (n = 5 per group) expressed as fold change in BDNF protein levels as compared to WT-V (* P < 0.05 vs WT-V; #P < 0.05 vs HRM-V; Bonferroni's test). β-actin is the loading control.