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Possible Cause of Postpartum Depression Pinpointed

Mouse study implicates GABA receptors in the central nervous system

By Jeffrey Perkel
HealthDay Reporter


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WEDNESDAY, July 30 (HealthDay News) -- Researchers have uncovered a potential cause for postpartum depression, at least in mice.

According to the study, from assistant researcher Jamie Maguire and lead researcher Istvan Mody, both of the David Geffen School of Medicine at the University of California, Los Angeles, dysregulation of a particular class of proteins called GABA receptors on the surface of certain neurons in the brain may induce post-delivery mood disorders ranging from "baby blues" to postpartum psychosis.

Text Continues Below



The findings immediately suggest a possible therapeutic intervention, the authors noted. They also provided researchers with a new animal model for studying the biology and treatment of the disease -- a valuable research tool that could accelerate the development of new treatments.

Yet the work was not performed in humans, stressed Dr. Bernard Carroll, scientific director of the Pacific Behavioral Research Foundation in California. Just because these animals appear to suffer from a disease akin to postpartum depression, he said, does not mean the two conditions are identical.

"We have to remember that the model is not the disease," he said.

The results were published in the July 31 issue of Neuron.

The protein at the heart of this study, the GABA receptor (type A), serves an inhibitory role in the nervous system, dampening the effect of excitatory neurotransmitters in response to its substrate, GABA. These receptors can bind to more than one molecule, however, and one particular class of molecules called neurosteroids can modulate the receptors' activity.

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.

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Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 7/30/2008

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SOURCES: Istvan Mody, Ph.D., Tony Coelho professor, neurology and physiology, department of neurology, David Geffen School of Medicine, UCLA; Jamie Maguire, Ph.D., assistant researcher, department of neurology, David Geffen School of Medicine, UCLA; Julio Licinio, M.D., professor and chairman, department of psychiatry and behavioral sciences, University of Miami Miller School of Medicine; Bernard Carroll, M.D., Ph.D., scientific director, Pacific Behavioral Research Foundation, Carmel, Calif.; July 31, 2008, Neuron


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