Effects of cysteamine in chronic corticosterone-treated mice on proBDNF and mature BDNF (mBDNF) protein levels in the frontal cortex and hippocampus.

<p>CD-1 male mice were treated for 7 weeks with vehicle (0.45% hydroxypropyl-β-cyclodextrin) or corticosterone (CORT; 35 ug/ml) in the presence or absence of cysteamine (CYS; 150 mg/kg/day) during the last three weeks of corticosterone treatment. proBDNF and mBDNF protein levels were determined in the (A) frontal cortex and (B) hippocampus by Western blot analysis. The upper panels shows a representative autoradiogram of proBDNF and mBDNF and the lower panel represents the fold change in optical density values normalized to vehicle-treated controls. β-actin was used as a protein loading control. Values are mean ± SE (n = 6 mice per group). (C) BDNF protein levels as measured by ELISA in frontal cortex samples from mice treated with vehicle or cysteamine for 3 weeks as above. Data represent the fold change in BDNF protein levels (pg/mg protein) normalized to vehicle-treated controls. Values are mean ± SE (n = 5 mice per group).</p

Effects of cysteamine in chronic corticosterone-treated mice on anxiety-like behaviors as measured in the (A-B) Light/Dark test, (C) Elevated Plus Maze Maze test and (D) Tail Suspension Test.

<p>CD-1 male mice were treated for 7 weeks with vehicle (0.45% hydroxypropyl-β-cyclodextrin) or corticosterone (CORT; 35 ug/ml) in the presence or absence of cysteamine (CYS; 150 mg/kg/day) during the last three weeks of the corticosterone treatment. (A) % of the time spent in the dark area, (B) % of the time spent in the lit area; (B) % of the number of entries in the open arms, and (D) the immobility score (in seconds). Values are mean ± SE (n = 8–9 mice per group). Bonferroni's post hoc test. *p<0.05 versus vehicle and ^#p<0.05 versus CORT.</p

Effects of chronic corticosterone treatment on TrkB mRNA levels in the frontal cortex and hippocampus.

<p>CD-1 male mice were treated with corticosterone (CORT; 35 ug/ml/day) or vehicle (0.45% hydroxypropyl-β-cyclodextrin) for 7 weeks. TrkB mRNA levels were determined by qRT-PCR analysis. The level of TrkB mRNA was normalized to that of RPS3 RNA in the same sample. Values are expressed as fold change relative to vehicle-treated mice. Open and filled bars represent vehicle and corticosterone-treated groups, respectively. Error bars represent standard Error (SE) of n = 4 mice per group.</p

Effects of chronic corticosterone treatment on TrkB protein levels in the hippocampus.

<p>CD-1 male mice were treated with corticosterone (CORT; 35 ug/ml/day) or vehicle (0.45% hydroxypropyl-β-cyclodextrin) for (A) 3, (B) 5 or (C) 7 weeks. TrkB protein levels were determined by Western blot analysis. The upper panel shows a representative autoradiogram of TrkB and the lower panel represents fold change in optical density values normalized to vehicle-treated controls. β-actin was used as a protein loading control. Values are mean ± SE (n = 5–6 mice per group). *p<0.05 versus vehicle.</p

Effects of chronic corticosterone treatment on TrkB protein levels in the frontal cortex.

<p>CD-1 male mice were treated with corticosterone (CORT; 35 ug/ml/day) or vehicle (0.45% hydroxypropyl-β-cyclodextrin) for (A) 3, (B) 5 or (C) 7 weeks. TrkB protein levels were determined by Western blot analysis. The upper panel shows a representative autoradiogram of TrkB and the lower panel represents the fold change in optical density values normalized to vehicle-treated controls. β-actin was used as a protein loading control. Values are mean ± SE (n = 5–6 mice per group). *p<0.05 versus vehicle.</p

Effects of cysteamine in chronic corticosterone-treated mice on TrkB protein levels in the frontal cortex and hippocampus.

<p>CD-1 male mice were treated for 7 weeks with vehicle (0.45% hydroxypropyl-β-cyclodextrin) or corticosterone (CORT; 35 ug/ml) in the presence or absence of cysteamine (CYS; 150 mg/kg/day) during the last three weeks of corticosterone treatment. TrkB protein levels were determined in the (A) frontal cortex and (B) hippocampus by Western blot analysis. The upper panel shows a representative autoradiogram of TrkB and the lower panel represents the fold change in optical density values normalized to vehicle-treated controls. β-Actin was used as a protein loading control. Values are mean ± SE (n = 5–6 mice per group). *p<0.05 versus vehicle and ^#p<0.05 versus CORT.</p

Effects of cysteamine in chronic corticosterone-treated mice in the Open Field test.

<p>CD-1 male mice were treated for 7 weeks with vehicle (0.45% hydroxypropyl-β-cyclodextrin) or corticosterone (CORT; 35 ug/ml) in the presence or absence of cysteamine (CYS; 150 mg/kg/day) during the last three weeks of the corticosterone treatment. (A) Mean total of the time-spent in the center for the entire session, (B) the ambulatory counts for each 5 min period, (C) the total ambulatory distance and (D) the ambulatory distance in the center over total. Values plotted are mean ± SEM (n = 8–10 per group). Bonferroni's post hoc test. *p<0.05 versus vehicle and ^#p<0.05 versus CORT.</p

Effects of cysteamine in TrkB knockout mice on anxiety-like behaviors as measured in the (A) Open Field test, (B-C) Light/Dark test, (D) Elevated Plus Maze Maze test and (E) Tail Suspension Test.

<p>TrkB knock out (KO) and wild type (WT) male mice were treated for 3 weeks with vehicle (water) or cysteamine (CYS; 150 mg/kg/day). (A) Mean total of the time spent in the center for the entire session, (B) % of the time-spent in the lit area, (C) % of the time-spent in the dark area, (D) % of the time in open arms, and (E) the immobility score (in seconds). Values are mean ± SE (n = 6 mice per group). Bonferroni's post hoc test. *p<0.05 versus vehicle.</p