| Literature DB >> 32187541 |
Eleni Siopi1, Grégoire Chevalier2, Lida Katsimpardi3, Soham Saha3, Mathilde Bigot3, Carine Moigneu3, Gérard Eberl2, Pierre-Marie Lledo4.
Abstract
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.Entities:
Keywords: 5-hydroxytryptophan; adult hippocampal neurogenesis; chronic stress; depression; fluoxetine; gut microbiota; serotonin; tryptophan
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Year: 2020 PMID: 32187541 DOI: 10.1016/j.celrep.2020.02.099
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423