Figure 6. TrkB^hGFAP mice were insensitive to chronic AD and exercise induced improvement in depression and anxiety-like behaviors.

(A) In the novelty-suppressed feeding test (NSFT), chronic treatments with fluoxetine or imipramine shortened the latency to feed (indicating reduced anxiety) in control, TrkB^Syn but not TrkB^hGFAP mice. Data were shown as percentage of control with saline injection. N=6–29 for each group. ANOVA (GLM) found significant effects of AD treatment (F_2,100=8.022, p=0.0006) and genotype (F_2,100=10.49, p<0.0001).

(B) The tail-suspension test (TST) measured total duration of immobility (“behavior despair”), which could be reduced by chronic fluoxetine or imipramine in control, TrkB^Syn but not TrkB^hGFAP mice. Data were shown as percentage of control with saline injection. N=7–28 for each. ANOVA (GLM) revealed significant effects of AD treatment (F_2,100=4.233, p=0.0172), genotype (F_2,100=20.03, p<0.0001) and the interaction of both (F_2,100=5.085, p=0.0009).

(C–D) Running for 6 weeks failed to increase the number of Ki67 (C) or Doublecortin (D) positive cells in the DG of TrkB^hGFAP mice. N=6–13 for each. ANOVA (GLM) revealed significant effects of running (F_1,36=13.64, p=0.0007 for Ki67; F_1,36=16.01, p=0.0003 for Doublecortin), genotype (F_1,36=141.1, p<0.0001 for Ki67; F_1,36=58.46, p<0.0001 for Doublecortin) and the interaction of the two (F_1,36=12.66, p=0.0010 for Ki67; F_1,36=14.79, p=0.0005 for Doublecortin).

(E–F) TrkB^hGFAP mice did not display decrease in latency to feed (E, NSFT) or duration of immobility (F, TST) after 6 weeks of running, compared to sedentary controls. Data were shown as percentage of sedentary control. N=8–16 for each. NSFT (F_1,41=15.09, p=0.0004 for genotype), TST (F_1,41=9.082, p=0.0044 for genotype; F_1,41=8.273, p=0.0064 for exercise).

*p<0.05; **p<0.01; ***p<0.001.