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Detection of G Protein-coupled Receptor Expression in Mouse Vagal Afferent Neurons using Multiplex In Situ Hybridization
Published on: September 20, 2021
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Gut bacteria interaction with vagal afferents.
Carolina R Cawthon1, Claire B de La Serre1
1Department of Foods and Nutrition, University of Georgia, 372 Dawson Hall, 305 Sanford Drive, Athens, GA 30602 USA.
Brain Research
|January 24, 2018
Summary
The gut microbiota influences host behavior and physiology by communicating with the brain via the vagus nerve. Disruptions in this gut-brain axis, particularly involving the nodose ganglion, can alter feeding behavior and contribute to metabolic disorders.
Area of Science:
- Neuroscience
- Microbiology
- Physiology
Background:
- The gut microbiota significantly impacts host physiology and can communicate with the central nervous system (CNS).
- Vagal afferent neurons, located in the nodose ganglion (NG), are crucial for relaying gut signals to the CNS, influencing behavior, including feeding.
- Microbiota alterations and inflammation in the NG are implicated in metabolic and behavioral disorders.
Purpose of the Study:
- To explore the communication pathways between the gut microbiota and the CNS via the vagus nerve.
- To investigate the role of nodose ganglion (NG) inflammation and microglia activation in microbiota-driven alterations of vagal signaling.
- To understand how microbiota dysbiosis affects feeding behavior and host energy balance.
Main Methods:
- Utilized germ-free models and next-generation sequencing to study gut microbiota dynamics.
- Investigated the effects of L. Rhamnosus supplementation and lipopolysaccharide (LPS) treatment on anxiety and feeding behavior in mice.
- Examined vagotomy effects and inflammation in the nodose ganglion (NG) following microbiota alterations or diet-induced dysbiosis.
- Assessed the impact of preventing dysbiosis and microglia activation on vagal innervation and energy intake in rodents.
Main Results:
- L. Rhamnosus supplementation reduced anxiety in mice, an effect abolished by vagotomy.
- Chronic LPS treatment impaired vagal feedback and increased food intake.
- Vagal damage and diet-driven microbiota dysbiosis were associated with NG microglia activation and altered vagal outputs.
- Preventing dysbiosis and microglia activation normalized vagal innervation and energy intake in high-fat diet-fed rodents.
Conclusions:
- Gut microbiota communicates with the CNS through the vagus nerve, influencing host behavior and physiology.
- Nodose ganglion (NG) inflammation and microglia activation are key mediators of microbiota-induced changes in vagal signaling and feeding behavior.
- Targeting microbiota-vagal communication and glial responses in the NG offers potential therapeutic strategies for metabolic and behavioral disorders.
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