New breakthrough in postpartum depression research

Neuroscientists at the Tufts University School of Medicine, US, have generated a novel preclinical model of postpartum depression.

In doing so, they have 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 researchers explained that postpartum depression affects almost one in five new mothers. They may experience anxiety, severe fatigue, inability to bond with their children and suicidal thoughts.

Postpartum depression has also been linked with infants’ developmental difficulties.

Stress is known to activate the HPA axis, which triggers the fight or flight response. During and after pregnancy such activation is typically blunted, which helps to insulate developing offspring from stress. It has been suggested that dysregulation of the HPA axis plays a role in the physiology of postpartum depression.

Research has not yet directly demonstrated a role for corticotropin-releasing hormone (CRH) - the main driver of the stress response, which is primarily secreted by a cluster of neurons in the hypothalamus called the paraventricular nucleus (PVN). Scientists have also not found a role for inappropriate activation of the HPA axis in postpartum depression.

Corresponding author of the new study Dr Jamie Maguire, assistant professor in the Department of Neuroscience at Tufts University School of Medicine, said: “Using a mouse model that we developed, our new study provides the first empirical evidence supporting the clinical observations of HPA axis dysfunction in patients with postpartum depression and 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 behaviours and deficits in maternal care.”ADNFCR-2094-ID-801843396-ADNFCR