According to Dr. Puttur D. Prasad, biochemist in the Medical College of Georgia School of Medicine, the crosstalk allows the mother's blood to flow out of the uterine artery and get just a single cell layer away from the foetus' blood.
This controlled exchange through placenta regulates the level of serotonin, a neurotransmitter commonly associated with depression.
But platelets that enable blood clotting also secrete serotonin, which prompts platelets to aggregate, and the placenta to want to get rid of it.
"If there were no proper control here, blood leaving the mother's blood vessel would trigger release of serotonin, platelets would aggregate, vessels constrict and the foetus wouldn't get what it needs," saidPrasad.
Dr Prasad also revealed that when the foetus and placenta are gone, blood continues flowing from the mother's uterine artery until platelets move in to stop it.
Serotonin levels begin to rise and interact with receptors on the smooth muscle of the uterus.
This stimulates production of interleukin-1 beta, which the MCG researchers found regulates expression of serotonin-hoarding transporters.
Interleukin-1 beta gets in the mother's bloodstream, crosses the blood brain barrier and creates more serotonin transporters on the neurons when they are not needed.
"We believe that 80 percent of women experience postpartum blues because of this effect of interleukin-1 beta. If our hypothesis holds true, lowering interleukin-1 beta levels may be a better treatment option," said Prasad.
In more serious postpartum depression, polymorphisms or variations of the serotonin transporter gene - which already have been linked to non-pregnancy related depression - appear to make bad matters worse because they are even better at taking up serotonin.