Pathophysiological mechanisms implicated in postpartum depression

Abstract

This review aims to summarize the diverse proposed pathophysiological mechanisms contributing to postpartum depression, highlighting both clinical and basic science research findings. The risk factors for developing postpartum depression are discussed, which may provide insight into potential neurobiological underpinnings. The evidence supporting a role for neuroendocrine changes, neuroinflammation, neurotransmitter alterations, circuit dysfunction, and the involvement of genetics and epigenetics in the pathophysiology of postpartum depression are discussed. This review integrates clinical and preclinical findings and highlights the diversity in the patient population, in which numerous pathophysiological changes may contribute to this disorder. Finally, we attempt to integrate these findings to understand how diverse neurobiological changes may contribute to a common pathological phenotype. This review is meant to serve as a comprehensive resource reviewing the proposed pathophysiological mechanisms underlying postpartum depression.

Chronic psychosocial stress during pregnancy affects maternal behavior and neuroendocrine function and modulates hypothalamic CRH and nuclear steroid receptor expression

“…Evidence gained through these models indicates peripartum stress results in the development of postpartum depressive-like behaviors 15,[27][28][29][30][31][32] , often associated with anxiety 15,30 , and can lead to quantitative alterations in maternal care 15,[27][28][29][30][31][32][33] . These changes are likely mediated by heightened CORT levels, as similar findings are reported after exogenous glucocorticoid administration during the peripartum period 34,35 . Abnormalities in maternal HPA axis circadian activity have also been noted following exposure to stress paradigms with psychosocial components 15,36 .…”

Psychological impact of COVID‐19 quarantine measures in northeastern Italy on mothers in the immediate postpartum period

“…Trauma, terrorist attack, and natural and man‐made disasters (e.g. earthquakes, tsunamis, and Chernobyl) were predictors of postpartum depression symptoms for mothers in the general population 4–6 . After the outbreak of severe acute respiratory syndrome (SARS) in 2003, both healthcare workers and people who were self‐quarantined exhibited symptoms of post‐traumatic stress disorder 7 .…”

Cerebellum-specific deletion of the GABAAreceptor δ subunit alters anxiety-like, social and maternal behaviors without affecting motor performance

“…Unexpectedly, we observed abnormal maternal care in cb  KO mice, including lack of interest in pups, failure to retrieve and increased cannibalization of pups (Figure 7). Given the strong connection between anxiety and stress in the genesis of postpartum depression (Camille Melón and Maguire, 2016;Payne and Maguire, 2019), the elevated levels of stress and anxiety in cb  KO mice are likely a major contributing fact to the observed abnormal maternal care in cb  KO mice. Our results suggest that some of the behavioral consequences on abnormal postpartum behaviors, like pup retrieval and cannibalization, are comparable for global KOs and cb  KO mice.…”