Journal
SCIENCE
Volume 311, Issue 5757, Pages 77-80Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1117571
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Funding
- NIDA NIH HHS [DA10044] Funding Source: Medline
- NIMH NIH HHS [MH40899] Funding Source: Medline
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The pathophysiology of depression remains enigmatic, although abnormalities in serotonin signaling have been implicated. We have found that the serotonin 113 receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11. p11 increases localization of 5-HT1B receptors at the cell surface. p11 is increased in rodent brains by antidepressants or electroconvulsive therapy, but decreased in an animal model of depression and in brain tissue from depressed patients. Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates certain behaviors seen after antidepressant treatment in mice. p11 knockout mice exhibit a depression-like phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reactions to an antidepressant.
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