Compared with the control group, CRS exposure significantly contributed to the increase in the expression of TLR4, MyD88, TRAF6, NF-κB p65, and TNF-α in the hippocampus (TLR4, F=16.748, P=0.000; MyD88, F=29.210, P=0.000; TRAF6, F=12.011, P=0.000; NF-κB p65, F=6.976, TNF-α, P=0.003; F=6.394, P=0.005; all P < 0.01), indicating the involvement of the stress-induced activation of neuroinflammation in the pathogenesis of depression. This evidence concerns the gene NFKB1 and depressive disorder.