Postpartum depression strikes nearly one in five new mothers, who may experience anxiety, severe fatigue, inability to bond with their children and suicidal thoughts.
Such depression has also been associated with infants' developmental difficulties.
Although stress has been identified as a significant risk factor for postpartum depression, this complex disorder is still poorly understood.
The study, published online in the journal Psychoneuroendocrinology, demonstrated the involvement of the neuroendocrine system that mediates physiological response to stress, called the hypothalamic-pituitary-adrenal (HPA) axis, which is normally suppressed during and after pregnancy.
The study "shows for the first time that dysregulation of the HPA axis and a specific protein in the brain, KCC2, can be enough to induce postpartum depression-like behaviour and deficits in maternal care," said study co-author Jamie Maguire, Assistant Professor at Tufts University School of Medicine in Boston, US.
The findings in mice provide a research model for further investigation into the causes of and treatment for postpartum depression, which has largely relied on co-relational studies in humans so far.
The study investigated the specific role of KCC2 in regulating the HPA axis during and after pregnancy.
Th researchers assessed the expression of the protein in brains of virgin, pregnant and postpartum mice.
They observed suppression (down regulation) of KCC2 in virgin mice exposed to stress but not in pregnant or postpartum mice.
(This story has not been edited by Social News XYZ staff and is auto-generated from a syndicated feed.)
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