Neural pathways for vomiting after consumption of contaminated food

Neural pathways for vomiting after consumption of contaminated food

Neural pathways for vomiting after consumption of contaminated food

Abstract: After consuming contaminated food, toxins activate the release of serotonin from enterochromaffin cells on the lining of the intestinal lumen. Serotonin binds to receptors on vagal sensory neurons in the gut, transmitting signals along the vagus nerve to neurons in the dorsal vagus complex, causing vomiting.

Source: Cell Press

The urge to vomit after eating contaminated food is the body’s natural defense response to get rid of bacterial toxins. However, the process of how our brain initiates this biological response after detecting germs remains elusive.

For the first time, researchers have mapped the detailed neural pathway of defense responses from the gut to the brain in mice.

The study was presented on November 1 in the journal Cellcould help scientists develop better anti-nausea drugs for cancer patients undergoing chemotherapy.

Many food-borne bacteria produce toxins in the host after ingestion. The brain, upon sensing their presence, will trigger a series of biological reactions, including vomiting and nausea, to get rid of the substance and develop an aversion to foods that taste or look the same.

“But the details of how the signals are transmitted from the gut to the brain have been unclear, because scientists have not been able to study the process in mice,” says Peng Cao, corresponding author of the paper at the National Institute of Biological Sciences in Beijing. Rodents cannot vomit, probably because of their long esophagus and lower muscle strength relative to their body size.

As a result, scientists have studied vomiting in other animals such as dogs and cats, but these animals have not been comprehensively studied and thus failed to discover the mechanism of nausea and vomiting.

Cao and his team noticed that while the mice don’t vomit, they do vomit—meaning they also feel the urge to vomit without vomiting.

The team found that after receiving staphylococcal enterotoxin A (SEA), a common bacterial toxin produced by Staphylococcus aureus that also causes foodborne illness in humans, the mice developed episodes of unusual mouth opening.

Mice that received SEA opened their mouths at greater angles than those observed in the control group, where mice received saline water. Moreover, during these episodes, the diaphragm and abdominal muscles of SEA-treated mice contract simultaneously, a pattern seen in dogs when they vomit. During normal breathing, the diaphragm and abdominal muscles of animals contract alternately.

“The neural mechanism of vomiting is similar to that of vomiting. “In this experiment, we have successfully built a paradigm for studying toxin-induced vomiting in mice, with which we can investigate the brain’s defense responses to toxins at the molecular and cellular levels,” says Cao.

In mice treated with SEA, the team found that the toxin in the intestines activated the release of serotonin, a type of neurotransmitter, from enterochromaffin cells lining the intestinal lumen.

Released serotonin binds to receptors on vagal sensory neurons located in the gut, which transmit signals along the vagus nerves from the gut to a specific type of neuron in the dorsal vagus complex—Tac1+DVC neurons—in the brainstem.

When Cao and his team deactivated Tac1+DVC neurons, SEA-treated mice vomited less compared to mice with normal Tac1+DVC neuron activity.

In addition, the team investigated whether chemotherapy drugs, which also cause defensive reactions such as nausea and vomiting in recipients, activate the same neural pathway.

Neural pathways for vomiting after consumption of contaminated food
Many food-borne bacteria produce toxins in the host after ingestion. The image is in the public domain

They injected the mice with doxorubicin, a common chemotherapy drug. The drug induced vomiting in the mice, but when the team deactivated their Tac1+ DVC neurons or serotonin synthesis in their enterochromaffin cells, the vomiting behavior of the animals was significantly reduced.

Cao says some of the current anti-nausea drugs for chemotherapy recipients, such as Granisetron, work by blocking serotonin receptors. The study helps explain why the drug works.

“With this study, we can now better understand the molecular and cellular mechanisms of nausea and vomiting, which will help us develop better drugs,” Cao says.

Next, Cao and his colleagues want to investigate how the toxins affect enterochromaffin cells. Preliminary research shows that enterochromaffin cells do not directly sense the presence of toxins. The process likely involves complex immune responses to damaged cells in the gut.

“In addition to food-borne bacteria, humans encounter many pathogens, and our bodies are equipped with similar mechanisms to expel these toxic substances.

“For example, a cough is our body’s attempt to remove the coronavirus. It’s a new and exciting field of research into how the brain senses the presence of pathogens and triggers responses to get rid of them,” Cao says, adding that future research may reveal new and better drug targets, including anti-nausea drugs.

See also

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About this neuroscience research news

Author: Press office
Source: Cell Press
Contact: Press office – Cell Press
Picture: The image is in the public domain

Original research: Open access.
A gut-to-brain axis for toxin-induced defense responses” Peng Cao et al. Cell


Abstract

A gut-to-brain axis for toxin-induced defense responses

Accents

  • Mice show nausea and vomiting to bacterial toxins and chemotherapy drugs
  • Identification of a molecularly defined gut-to-brain circuit for nausea and vomiting
  • Different circuits of the brain stem stimulate nausea and vomiting
  • Toxin-induced signals can be mediated through the immune-neuroendocrine axis in the gut

Abstract

After ingesting food contaminated with toxins, the brain initiates a series of defensive reactions (eg, nausea, vomiting, and retching). How the brain detects an ingested toxin and coordinates various defense responses remains poorly understood.

Here, we developed a mouse-based paradigm to study defense responses induced by bacterial toxins. Using this paradigm, we identified a set of molecularly defined gut-to-brain and brain circuits that collectively mediate toxin-induced defense responses.

The gut-to-brain circuit consists of a subset Htr3a+ vagal sensory neurons that transmit toxin-related signals from intestinal enterochromaffin cells to Tac1+ neurons in the dorsal vagus complex (DVC).

Tac1+ DVC neurons trigger vomiting-like behavior and conditioned taste avoidance via divergent projections to the rostral ventral respiratory group, i.e. the lateral parabrachial nucleus. Manipulating these circuits also interferes with defense responses induced by the chemotherapy drug doxorubicin.

These results suggest that food poisoning and chemotherapy recruit similar circuit modules to initiate defense responses.

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