Summary: New study provides concrete proof that the vagus nerve serves as the gateway to communication between the gut bacteria and the brain. Using germ-free animals, scientists observed considerably reduced serotonergic brain action, which returned to normal after introducing colon bacteria.
When regular mice were treated with antibiotics to kill bacteria, serotonergic activity decreased, but it returned when microbiome-derived bowel fluids were reintroduced. Specific compounds, including short-chain fatty acid and bile acid, were identified as important activators of serotonergic neurons.
These indicators extended to the brain, confirming a distinct gut-to-brain route. The findings improve our understanding of the gut-brain shaft and may provide new therapies for neural and digestive conditions.
Major Information
- Gut-Bacteria Link: Germ-free animals had reduced serotonergic brain activity, restored just when gut microbes were introduced.
- Metabolite Activation: Short-chain fatty acid and bile acid from the gut microbiome immediately stimulated vagus nerve action.
- Healing Potential: Understanding vagal-mediated gut-brain conversation may help develop treatments for neural and gut-related conditions.
Origin: UCLA
A recent study in an animal model addresses a significant gap in the field by providing strong proof for the parasympathetic nerve’s role in colon microbiome-brain communication.
The study, led by , Kelly G.  , Jameson while a PhD student in the Hsiao Lab at UCLA, demonstrates a distinct direct connection between gut microbiome and serotonergic brain activity.
Although it has long been believed that the gut microbiome, a group of microorganisms living in the intestines, communicates with the brain, primary evidence for this activity has been lacking.
Experts led by Jameson found that germ-free mice, mice raised without any gut bacteria, had significantly lower exercise in their parasympathetic nerves compared to mice with normal gut microbiomes. Importantly, when these germ-free mice were exposed to normal gut bacteria, their nociceptive brain activity increased to levels that were standard.
In addition, in addition to introducing antibiotics into regular mice’s small intestines, this experiment resulted in a decrease in serotonergic exercise. In germ-free animals, medicines had no impact on serotonergic activity.
The serotonergic action was restored when the antibiotics were removed and replaced with the bowel fluids from healthy mice. This repair did not occur using fluids from germ-free mice, which highlights the crucial function of the bacteria.
Additionally, the study identified certain substances produced by the gut bacteria, such as short-chain fatty acids and liver acids, that may induce serotonergic action by acting on certain receptors.
Different groups of vagus nerve cells were activated by these compounds, each with its own distinct response pattern. This detection extended to neurons in the brain, demonstrating a distinct pathway for gut-brain conversation.
The study demonstrated that the gut microbiome regulates some compounds that activate the vagus nerve, facilitating the distribution of chemosensory signals from the intestines to the head, improving the knowledge of the gut-brain shaft, and creating new avenues for research into treatments for neural and digestive disorders.
About this news from neuroscience research
Author: David Sampson
Source: UCLA
Contact: David Sampson – UCLA
Image: The image is credited to Neuroscience News
Original Research: Open access.
” The small intestinal lumen’s selection of microbial metabolites regulates vagal activity via receptor-mediated signaling.” by Kelly G.  , Jameson et al. iScience
Abstract
The small intestinal lumen’s selection of microbial metabolites regulates vagal activity via receptor-mediated signaling.
Activity-based evidence is lacking, but it is suggested that the gut microbiome and the brain communicate via the vagus nerve. We discover that germ-free mice exhibit a lower vagal tone than colonized controls, which is reversed by microbiota restoration.
Perfusing antibiotics into the small intestines of conventional mice, but not germ-free mice, acutely decreases vagal activity which is restored upon re-perfusion with intestinal filtrates from conventional, but not germ-free, mice.
Microbiome-dependent short-chain fatty acids, bile acids, and 3-indoxyl sulfate indirectly stimulate vagal activity in a receptor-dependent manner.
Each metabolite class’s serial perfusion triggers both distinct and shared neuronal subsets with different response kinetics.
Metabolite-induced and receptor-dependent increases in vagal activity correspond with the activation of brainstem neurons.
The gut microbiome controls a number of metabolites in the intestinal lumen that can differentially activate vagal afferent neurons, enabling microbial modulation of chemosensory signals for gut-brain communication, according to the findings of this study.
