Mice genetically deficient in serotonin -- a crucial brain chemical implicated in clinical depression -- are more vulnerable than their normal littermates to social stressors, according to a Duke study appearing this week in the Proceedings of the National Academy of Sciences.
Following exposure to stress, the serotonin-deficient mice also did not respond to a standard antidepressant, fluoxetine (Prozac), which works by boosting serotonin transmission between neighboring neurons.
The new results may help explain why some people with depression seem unresponsive to treatment with selective serotonin reuptake inhibitors (SSRIs), the most common antidepressant drugs on the market today. The findings also point to several possible therapeutic strategies to explore for treatment-resistant depression.
“Our results are very exciting because they establish in a genetically defined animal model of serotonin deficiency, that low serotonin could be a contributing factor to the development of depression in response to psychosocial stress -- and can lead to the failure of SSRIs to alleviate symptoms of depression,” said senior author Marc Caron, the James B. Duke professor of cell biology in the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences.
The exact causes of depression are unclear. Although scientists have traditionally thought that low brain serotonin could cause depression, the idea is difficult to test directly and increasingly controversial. At the same time, researchers have gained a greater appreciation for the many environmental factors -- especially stress -- that can bring on or worsen depression.
Category(s):Social Anxiety / Phobia
Source material from Duke University
