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.
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