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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 4.

Fig 4

Cysteamine treatment ameliorates the reduction in TrkB 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 4A and 4B) or 30 (Figs 4C and 4D) days. TrkB expression was determined by western blot analysis in frontal cortex (Figs 4A and 4C) and hippocampus (Figs 4B and 4D). 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. Data represent mean±SE (n = 5 per group) expressed as fold change in TrkB 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.