The study presented investigates how concurrent intake of antidepressants and anti-inflammatories modulate p11 levels in the body. p11 is a small regulatory protein of selective serotonin reuptake inhibitors (SSRIs). Past studies have linked low p11 levels to depressive like symptoms and higher levels of p11 to antidepressant activities. This was shown using p11 knockout mice and mice that were induced to express more p11.
In the context of the paper, they claim that p11 regulates some sertonin receptors by modulating their respective cell trafficking and localization in cell membranes. Doing such actions lead to different behaviour
The anti-depressants citralopram and fluoextin were shown to increase levels of p11 in mouse models. Coadministration of an NSAID with citralopram and fluoextine did not increase p11 levels.
Furthermore, the Tail suspension test (TST) and the forced swim test (FST) were administered to determine any change in depressive behavior in mice. Mice that were taking NSAIDs in addition to antidepressants scored more poorly than those that did not take NSAIDs.
The authors also investigated what cytokines are linked to increased levels of p11. TNF-a and IFN-g were injected into the frontal lobe of mice brain and western blot analysis revealed that mice injected with these cytokine yielded higher p11 levels compared to controls. This supports the idea that inflammation is involved with depression.
Based on the data, the authors feel that concurrent treatment of pain with NSAIDs and SSRI antidepressants minimizes the improvement of depressive symptoms.
Paper title: Antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) are attenuated by antiinflammatory drugs in mice and humans
paper published online 4-25-11
link to paper: http://www.pnas.org.ezproxy2.library.arizona.edu/content/early/2011/04/20/1104836108.long
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