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. 2010 Jul 28;5(7):e11825. doi: 10.1371/journal.pone.0011825

Figure 2. Transient activation of Trp catabolism after acute psychological stress.

Figure 2

A–E. Kinetics of IDO1 mRNA expression induced in brain (A), lung (B), spleen (C) and Peyer's patches (D) within 24-h after termination of 2-h-stress exposure (n = 6 mice/time, n = 6 controls; average values of basal expression levels in non-stressed mice were assigned as value of 1), and IDO1 mRNA expression in the brain of TNFα antiserum- and IFNγ antiserum treated vs. vehicle-treated animals 6-h after acute stress (E, n = 6 mice/group, average values of basal expression levels in vehicle treated, non-stressed mice assigned as value of 1). F–I. Kinetics of plasma concentrations of Trp (F), Kyn (G), the Kyn/Trp ratio (H) and of the levels of serotonin (I), Quin (J) and Kyna (K) following 2-h-stress exposure (n = 6 mice/time) compared with basal levels of healthy controls (n = 15 mice/group). All panels depict data of one representative experiment of two: *p<.05; **p<.01; ***p<.001 compared with non-stressed controls; #p<.05; ##p<.01; ###p<.001 compared with mice immediately after acute stress (0-h) and ⊥<.05 ⊥⊥<0.01, ⊥⊥⊥<0.001 compared with mice 24-h after stress exposure by Kruskal-Wallis testing with post-hoc Dunn Multiple comparison testing (KW- and p-values are indicated in the graph).