The news is popping up all over today about a study in the July 31 issue of Neuron that appears to have uncovered a potential cause for postpartum depression, at least in mice. Warning — I have no idea how to translate the following into language for lay people. Trust me, I've searched the web and not a single site explains this for plain folk like myself. If anyone out there understands neuroscientist researcher speak, let me know …
Per Healthday: According to the study, conducted by assistant researcher Jamie Maguire and lead researcher Istvan Mody from the David Geffen School of Medicine at the University of California, Los Angeles, dysregulation of proteins called GABA receptors on the surface of certain neurons in the brain may bring on mood disorders after birth ranging from "baby blues" to postpartum psychosis …
Neurosteroids are produced in the central nervous system from steroid hormones such as progesterone. During pregnancy, the levels of reproductive hormones (including progesterone) rise sharply, only to drop to pre-pregnancy levels shortly after delivery. As a result, neurosteroid levels also rise and fall.
Maguire and Mody wanted to see what happens to GABA receptors in the brains of mice undergoing the hormonal swings associated with pregnancy. By comparing virgin, pregnant and postpartum mice, the pair discovered that GABA receptor abundance (and function) falls during pregnancy and then returns to pre-pregnancy levels following birth.
For the body to maintain a constant level of GABA receptor-derived inhibition, receptor abundance must stay more or less in sync with neurosteroid levels.
"If you want to maintain a constant level of inhibition, with more neurosteroids, you need fewer receptors," she explained. "After pregnancy, when hormone levels drop off, you need more receptors to maintain that level. If you cannot maintain that level after pregnancy, that's when the disorders manifest."
She and Mody reached that conclusion using mice genetically engineered to lack a particular component of the GABA receptor — that is, mice that cannot adjust GABA receptor levels in response to changing hormone levels. By comparing these mutants to normal mice, the pair discovered that dysregulation of the normal changes in GABA receptor levels lead to mouse behaviors akin to postpartum depression, such as anxiety and depression, with a concomitant decrease in pup survival.
Treatment with THIP (Gaboxadol), a GABA receptor agonist originally intended to treat sleep disorders, ameliorated these effects in mice containing decreased levels of GABA receptors.
"Our thinking is that postpartum depression, and maybe premenstrual syndrome and premenstrual dysphoric disorder, may be due to impaired trafficking of these [GABA] receptors to the [neural] membrane," Mody said.
The next step, he said, is to determine whether human postpartum depression is caused by a similar defect.
"We don't know if this is the same mechanism in humans, but I think all indications are there," Mody said. "The women that are affected by the disorder, the hormone levels are not changed, they are not different than in unaffected women. So, we are confident that it must be the receptor trafficking mechanism that is affected, because the changes in hormone levels are pretty normal."
Click here for more information on the causes of postpartum depression.
