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Jyoti Pal Published on July 31, 2008 - 0 comments
Researchers at the University of California, Los Angeles, claim to have developed a brain model that holds the clue for a potential cause of postpartum depressiondefine, at least in mice. The absence of GABA receptor (type A) – a chemical receptor in the brains of the mice is believed to be the basis of the post-delivery mood disorders, the researchers found.
Replicating the findings from the new animal model onto humans, researchers hope to better understand why nearly 25 percent of all new mothers are thought to suffer some form of post-natal depressiondefine. The research could also act as a tool that could accelerate the development of new treatments.
For the study, researchers focused on a chemical messaging system in the brains of the mice. GABA receptor (type A) - already known to play a key part in the regulation of mood and anxiety decreased the activity of certain nerve cells ones it came into contact with receptors on that cell's surface, researchers traced.
The genetically engineered new mouse mothers were more sluggish and less pleasure-seeking, much like human mothers suffering from postpartum depression. The depression like behavior also lead to new-mothers shunning their new-borns.
"After giving birth, female mice deficient in the suspect protein showed depression-like behaviors and neglected their newborn pups," explained Istvan Mody, lead researcher of the study.
However, this abnormal maternal behavior markedly improved and pup mortality rate reduced when these animal mothers were administered a drug called THIP.
"Giving a drug that restored the protein's function improved maternal behavior and reduced pup mortality," Mody said.
"Improper functioning of the subunit could impair the GABA system's ability to adapt to hormone fluctuations during the highly vulnerable post partum period," explained Dr Jamie Maguire, co-researcher for the study. "Targeting this subunit might be a promising strategy in developing new treatments for postpartum depression," Maguire emphasized.
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