A week or so ago we learned that researchers at UCLA uncovered that mice lacking a certain protein (remember GABA?) were depressed and neglected their babies. When the protein was reintroduced it restored the mama mice to normal maternal behavior.
This week, a different study out of the Medical College of Georgia finds that something called "crosstalk" may help identify the cause of baby blues and postpartum depression. Crosstalk is the term used to define the exchange of nutrition and oxygen from mother to child during pregnancy in blood traveling through the placenta.
Platelets that enable blood clotting secrete serotonin. Apparently the serotonin prompts the clotting. This leads the placenta to try and get rid of the serotonin so that blood vessels don’t constrict and prevent the fetus from getting all that it needs. A serotonin transporter gene prevents clotting until after birth.
Once the fetus and placenta are delivered, platelets then move in to stop unterine bleeding. Serotonin released by those platelets leads serotonin levels to rise, which stimulates production of interleukin-1 beta, another type of protein. 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. Why is that a problem? Because serotonin transporters reuptake serotonin and terminate its function. That’s not what we need, because serotonin helps regulate mood, sleep and appetite.
Until interleukin-1 beta levels normalize, there’s too little communication between serotonergic neurons and moms get the blues, says researcher Dr. Puttur Prasad.
In more serious postpartum depression, 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, he says. Which means we have even less. Yikes.
Dr. Prasad now plans to analyze DNA to see if women identified with postpartum depression have some of the same variations of the serotonin transporter gene already identified with non-pregnancy related depression.
