Journal
CELL REPORTS
Volume 30, Issue 11, Pages 3682-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.02.099
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Funding
- Investissements d'Avenir program [ANR-11-IDEX-0004-02, ANR-10-LABX-73]
- Agence Nationale de la Recherche [ANR-15-CE37-0004-01]
- AG2R La Mondiale
- Mutuelle de la Region Lyonnaise
- Fondation des Gueules Cassees
- Labex Revive
- Ecole des Neurosciences de Paris
- Agence Nationale de la Recherche (ANR) [ANR-15-CE37-0004] Funding Source: Agence Nationale de la Recherche (ANR)
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Major depressive disorders (MDDs) constitute a leading cause of disability worldwide and current pharmacological treatments are partially effective. The gut microbiota (GM) has recently emerged as a target of therapeutic interest for MDDs. In this study, we transfer GM from mice that sustained unpredictable chronic mild stress (UCMS) to healthy recipient mice. The fecal transfer induces despair-like behavior, decreases neurogenesis in the hippocampus (HpC), and impairs the antidepressant and neurogenic effects of a standard selective serotonin (5-HT) reuptake inhibitor, fluoxetine (FLX). These effects are paralleled by deficits in 5-HT bioavailability, biosynthesis, and reuptake in the HpC. Treatment with 5-hydroxytryptophan restores the levels of 5-HT and its precursors in the HpC, improves HpC neurogenesis, and alleviates despair-like symptoms. Our results reveal that stress-induced changes in GM are involved in the pathogenesis of depressive disorders and minimize FLX efficacy via alterations in the serotonergic pathway of Trp metabolism.
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