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Home | Pregnancy Timeline | News Alerts |News Archive Sep 3, 2013
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Shutting off neurons helps bullied mice overcome symptoms of depression Findings point to new potential drug target—GABA neurons—to treat patients with depression and other mood disorders. A new drug target to treat mood disorders such as depression, may lie in a group of GABA neurons (gamma-aminobutyric acid, the neurotransmitters which inhibit other cells) shown to contribute to symptoms like social withdrawal and increased anxiety, Penn Medicine researchers report in a new study in the Journal of Neuroscience. Experts know that people suffering from depression and other mood disorders often react to rejection or bullying by withdrawing themselves socially more than the average person who takes it in strides, yet the biological processes behind these responses have remained unclear. Using a mouse model, scientists identified bullying and other social stress symptoms triggered by depression, were activated by GABA neurons. A direct relationship between social stimuli and this neural circuitry comes from the lab of Olivier Berton, PhD, assistant professor, department of Psychiatry, collaboratng with Sheryl Beck, PhD, professor, department of Anesthesiology, both at the Children's Hospital of Philadelphia. Conversely, when the researchers successfully 'quieted' the effect of GABA neurons, mice became more resilient to bullying and didn't avoid previously perceived threats.
Reduced serotonin production elicits socially defensive responses such as avoidance and/or submission, where as enhancing serotonin production—the intended goal of antidepressants—induces a positive perception of social effectiveness, promoting affiliation and dominance. By comparing gene expression in the brains of resilient and avoidant mice, Berton and colleagues discovered that bullying in avoidant mice puts GABA neurons in an 'excited' state with mice exhibiting signs of social defeat. Resilient mice, however, had no change in neuron levels or behavior. Current antidepressants targeting serotonin, such as SSRIs, are only effective in about 50 percent of patients. With the current findings, new treatments for SSRI non-responsive patients may be able to be developed.
"Our paper provides a novel cellular understanding of how social defensiveness and social withdrawal develop in mice and gives us a stepping stone to better understand the basis of similar social symptoms in humans," said Berton. "This has important implications for the understanding and treatment of mood disorders." Abstract This work was funded by the National Institute of Mental Health grants MH087581, MH0754047 and MH089800 and grants from the International Mental Health Research Organization, the National Alliance for Research on Schizophrenia and Depression and the National Institute on Drug Abuse. Co-authors on the study include Collin Challis, Janette Boulden, Avin Veerakumar, Julie Espallergues, and R. Christopher Pierce from Penn's department of Psychiatry. Original press release:http://www.uphs.upenn.edu/news/News_Releases/2013/08/berton/ |