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. 2020 Oct 7;8:867. doi: 10.3389/fcell.2020.00867

FIGURE 1.

FIGURE 1

Early life stress-induced alterations of three depressive-related paths, the HPA axis, 5-HT, and BNDF, respectively due to epigenetic modification. 1) Early life stress impaired the GRs and paralleled with the dysfunctional negative feedback loop of the HPA axis. Specifically, the enhanced expression of CRH and ACTH, and abundant glucocorticoid was observed. Moreover, AVP, POMC, and FKBP5 KITLG collaborated to regulate the function of HPA axis.2) Early life stress primarily weakened the activity of 5-HTT but enhanced MAO activity. Therefore, early life stress suppressed the recycling of 5-HT and facilitated its degradation. 3) Early life stress inhibited the BDNF and TrkB and indirectly impaired the neurogenesis and neuroplasticity via AKT, CAMK, and ERK pathways. Abbreviation: CRH: corticotrophin-releasing hormone; AVP: arginine vasopressin, ACTH: adrenocorticotropic hormone; POMC: proopiomelanocortin, GR: glucocorticoid receptor; 5-HT: 5-hydroxytryptamine; 5-HTT: serotonin transporter; BDNF: brain-derived neurotrophic factor; TrkB: tropomyosin receptor kinase B; CAMK: calmodulin-dependent kinase, FKBP5: FK506 binding protein 5, KITLG: Kit ligand gene.