Antibiotic treatment-induced dysbiosis differently affects BDNF and TrkB expression in the brain and in the gut of juvenile mice

• DOI: 10.1371/journal.pone.0212856
• Publication Date: 2019-02-22T18:54:10Z
• Authors: Michela Bistoletti; Valentina Caputi; Nicolò Baranzini; Nicoletta Marchesi; Viviana Filpa; Ilaria Marsilio; Silvia Cerantola; Genciana Terova; Andreina Baj; Annalisa Grimaldi; Alessia Pascale; Gianmario Frigo; Francesca Crema; Maria Cecilia Giron; Cristina Giaroni
• Keywords: Trk receptor; Gut–brain axis

Antibiotic use during adolescence may result in dysbiosis-induced neuronal vulnerability both the enteric nervous system (ENS) and central (CNS) contributing to onset of chronic gastrointestinal disorders, such as irritable bowel syndrome (IBS), showing significant psychiatric comorbidity. Intestinal microbiota alterations influence expression molecular factors involved development ENS CNS. In this study, we have evaluated brain-derived neurotrophic factor (BDNF) its high-affinity receptor tropomyosin-related kinase B (TrkB) juvenile mice CNS, after a 2-week antibiotic (ABX) treatment. mucosa mucosa-deprived whole-wall small intestine segments ABX-treated animals, BDNF TrKB mRNA protein levels significantly increased. longitudinal muscle-myenteric plexus preparations percentage myenteric neurons staining for TrkB was higher than controls. After ABX treatment, consistent population BDNF- TrkB-immunoreactive costained with SP CGRP, suggesting up-regulation signaling motor sensory neurons. were downregulated hippocampus remained unchanged prefrontal cortex animals. Immunostaining decreased CA3 dentate gyrus subregions, respectively, cortex. These data suggest that dysbiosis differentially influences BDNF-TrkB Such changes potentially contribute later functional gut IBS,