In an additional experiment, the "depressed" mice were randomly divided into treatment groups. Some mice were treated with fluoxetine, the antidepressant marketed as Prozac, and some mice were treated with haloperidol, a psychotropic drug used to treat anxiety, addiction, and depression. To determine the effectiveness of each therapy, mice were subjected to repeating the forced swimming, staircase, and rotarod tests. Depression-like behavior was significantly blocked by long-term treatment with fluoxetine, but not by short- or long-term treatment with haloperidol.
At the culmination of the experiments, the brains of mice were sectioned and scrutinized through immunostaining. The staining pattern delineated the limbic system, which regulates the automatic nervous system’s response to stress. It also highlighted areas of the brain associated with the sense of smell.
These findings provide a novel line of research into the mechanisms underlying the limbic and olfactory pathways in depression. Imaging studies both in patients with clinical depression and patients with SLE could help determine whether these pathways are similarly affected in humans.
"The relevance of the results to the involvement of the central nervous system in SLE is another intriguing aspect of the present study," notes its leading author, Yehuda Shoenfeld, M.D., while emphasizing the need for further investigation through large-scale clinical studies. "Elucidating the mechanisms by which anti-ribosomal P induces behavioral changes may lead to novel therapeutic advances for SLE patients with depression," Dr. Shoenfeld reflects.
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Source:John Wiley & Sons, Inc.