After ingesting food contaminated with bacterial toxins, the brain initiates a series of defensive responses. These include motor reflexes such as gagging and vomiting, which promote expulsion, and unpleasant sensations called “gagging,” which serve as a learning signal for conditioned avoidance of taste to prevent future ingestion of the same toxin.

Paradoxically, these responses are the leading cause of the severe side effects of chemotherapy drugs. Using competent animal models for emesis, studies suggest that a gut-brain axis is involved.

For the first time, researchers at the National Institute of Biological Sciences in Beijing, China, traced the detailed neural pathway of defensive responses from the gut to the brain in mice. Many foodborne bacteria produce toxins in the host after being ingested.

The team realized that although the mice don’t vomit, they gag, meaning they also experience the urge to vomit. The team found that after receiving staphylococcal enterotoxin A (SEA), a common bacterial toxin produced by Staphylococcus aureus, which also causes foodborne illness in humans, the mice developed episodes of unusual mouth opening at wider angles than those observed in the control group. Furthermore, during these episodes, the diaphragm and abdominal muscles of the SEA-treated mice contract simultaneously, a pattern seen in dogs when they are vomiting.

They found that the toxin in the gut triggers the release of serotonin, a type of neurotransmitter, from enterochromaffin cells in the lining of the gut lumen. The released serotonin binds to receptors on vagal sensory neurons located in the gut, which transmit signals along the gut’s vagus nerves to a specific type of dorsal vagal complex neuron – Tac1+DVC neurons – in the gut. Brainstem. When Tac1+DVC neurons were inactivated, SEA-treated mice retched less than mice with normal activities.

In addition, the team investigated whether chemotherapy drugs, which also induce defensive responses such as nausea and vomiting in recipients, activate the same neural pathway. They injected (the mice) doxorubicin, a standard chemotherapy drug. The drug caused retching, but when the team inactivated their Tac1+ DVC neurons or serotonin synthesis from their enterochromaffin cells, it was significantly reduced.


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