�Researchers hold pinpointed a mechanism in the brains of mice that could explain why some human mothers turn depressed following childbirth. The discovery could lead to improved treatment for postpartum depression. Supported in part by the National Institute of Mental Health, of the National Institutes of Health, the study used genetically engineered mice wanting a protein critical for adapting to the sexual urge hormone fluctuations of gestation and the postpartum period.
"For the commencement time, we may own a highly useful poser of postnatal depression," said NIMH Director Thomas R. Insel, M.D. "The new research likewise points to a specific potential new target in the brain for medications to regale this disorder that affects 15 pct of women after they give birth."
"After giving birth, female mice deficient in the mistrust protein showed depression-like behaviors and unattended their new-sprung pups," explained Istvan Mody, Ph.D., of the University of California at Los Angeles, world Health Organization led the research. "Giving a dose that restored the protein's function improved maternal behavior and reduced pup mortality."
Mody and Jamie Maguire, Ph.D., report on their findings in the July 31, 2008 issuance of Neuron.
Researchers had suspected that postnatal depression cauline from the marked fluctuations in estrogen and lipo-Lutin that go with pregnancy and childbirth. Yet manipulating the hormones experimentally triggers great Depression only in women with a history of the disorder. The roots of their vulnerability remain a mystery.
Evidence suggested that the hormones exert their personal effects on mood through the brain's major inhibitory chemical messenger organisation, called GABA, which dampens neural activity, helping to regulate when a neuron fires.
Mody and Maguire ascertained that a GABA sensory receptor subunit fluctuated conspicuously during pregnancy and postpartum in the brains of female mice, hinting that it might have pivotal behavioral effects. To find knocked out, they used mice deficient the factor for this subunit and studied them in situations that can elicit responses similar to human depression and anxiety.
Much like human mothers suffering from postnatal depression, the genetically altered mouse mothers were more than lethargic and less pleasure-seeking than normal mice. They also shunned their pups and failed to make proper nests for them.
This abnormal maternal behavior was reversed and pup survival increased after the researchers gave the animals a drug called THIP that acts on the sensory receptor in a way that specifically restores its function in spite of the reduced numeral of subunits.
"Improper functioning of the subunit could impair the GABA system's ability to adapt to internal secretion fluctuations during the extremely vulnerable post partum period," explained Maguire. "Targeting this subunit might be a promising strategy in development new treatments for postnatal depression."
Reference:
Maguire J, Mody I. GABAAR plasticity during maternity: relevance to postpartum great Depression. Neuron. 2008 Jul 31;
The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, learning ability, and behaviour. More data is available at the NIMH website, http://www.nimh.nih.gov/.
The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a portion of the U.S. Department of Health and Human Services. It is the primary union agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more selective information about NIH and its programs, call in http://www.nih.gov/.
Source: Jules Asher
NIH/National Institute of Mental Health
More info
