Microbial Reconstitution Reverses Maternal Diet- Induced Social and Synaptic Deficits in Offspring

Publication

Cell

Author(s)

Shelly A. Buffington,
Gonzalo Viana Di Prisco,
Thomas A. Auchtung, Nadim J. Ajami, Joseph F. Petrosino,
Mauro Costa-Mattioli

Abstract

In brief:
A maternal high-fat diet leads to changes in the gut microbiome of offspring and induces behavioral alterations that can be restored via selective reintroduction of a commensal bacterial strain.

Summary:
Maternal obesity during pregnancy has been associated with increased risk of neurodevelopmental disorders, including autism spectrum disorder (ASD), in offspring. Here, we report that maternal high-fat diet (MHFD) induces a shift in microbial ecology that negatively impacts offspring social behavior. Social deficits and gut microbiota dysbiosis in MHFD offspring are prevented by co-housing with offspring of mothers on a regular diet (MRD) and transferable to germ-free mice. In addition, social interaction induces synaptic potentiation (LTP) in the ventral tegmental area (VTA) of MRD, but not MHFD offspring. Moreover, MHFD offspring had fewer oxytocin immunoreactive neurons in the hypothalamus. Using metagenomics and precision microbiota reconstitution, we identified a single commensal strain that corrects oxytocin levels, LTP, and social deficits in MHFD offspring. Our findings causally link maternal diet, gut microbial imbalance, VTA plasticity, and behavior and suggest that probiotic treatment may relieve specific behavioral abnormalities associated with neurodevelopmental disorders.

Date

June 16, 2016

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