In another study that employed a CUMS-induced mouse animal model of depression, Yang and collaborators [27] demonstrated that chronic stress significantly elevated proBDNF, p75NTR, and sortilin levels, while decreasing mature BDNF/TrkB levels in the cortex and hippocampus of mice, providing evidence that there is an imbalance between proBDNF/p75NTR/sortilin and BDNF/TrkB in the pathogenesis of depression, and it can, to some extent, be reversed by antidepressant treatment. This evidence concerns the gene NGFR and major depressive disorder.