Accordingly, as shown in Figure 3c, the restraint stress induced an increase in the phosphorylated form of the TRKB receptor in the Tyr706 (+57%, p < 0.05 vs. No stress/No ARS, Fisher’s PLSD) (CRSxARS interaction F1-20 = 4.687, p < 0.05, two-way ANOVA), an effect that was completely paralleled by the upregulation of the TRKB full-length form in control animals (+121%, p < 0.01 vs. No stress/No ARS, Fisher’s PLSD) but not in animals previously exposed to CRS (Figure 3d), whereas we did not observe any modulation for the truncated form of the receptor (Figure 3e). The gene discussed is NTRK2; the disease is congenital rubella syndrome.