Contemporary techniques including the use of germ-free models and next generation sequencing have deepened our understanding of the gut microbiota dynamics and its influence on host physiology. There is accumulating evidence that the gut microbiota can communicate to the CNS and is involved in the development of metabolic and behavioral disorders.

Vagal afferent terminals are positioned beneath the gut epithelium where they can receive, directly or indirectly, signals produced by the gut microbiota, to affect host behavior, including feeding behavior.

Supplementation with L. Rhamnosus in mice notably causes a decrease in anxiety and these effects are abolished by vagotomy. Additionally, chronic treatment with bacterial byproduct lipopolysaccharide (LPS) blunts vagally-mediated post-ingestive feedback and is associated with increased food intake. Inflammation in the nodose ganglion (NG), the location of vagal afferent neurons’ cell bodies, may be a key triggering factor of microbiota-driven vagal alteration. Interestingly, several models show that vagal damage leads to an increase in immune cell (microglia) activation in the NG and remodeling of the vagal pathway. Similarly, diet-driven microbiota dysbiosis is associated with NG microglia activation and decreased vagal outputs to the CNS. Crucially, preventing dysbiosis and microglia activation in high-fat diet fed rodents normalizes vagal innervation and energy intake, highlighting the importance of microbiota/vagal communication in controlling feeding behavior.

As of today, new consideration of potential roles for glial influence on vagal communication and new methods of vagal afferent ablation open opportunities to increase our understanding of how the gut microbiota influence its host’s health and behavior.