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Cell was once bitten by a snake, ten years afraid of the well rope! Cao Peng/Xie Zhiyong/Shang found the internal organs of the toxin-induced defense response to the brain axis from equal

 Last Update: 2022-11-04
 Source: Internet
 Author: User

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After ingesting toxin-contaminated food, the brain initiates a series of defensive responses such as nausea, retching, and vomiting
.
How the brain detects ingested toxins and coordinates different defense responses remains unclear
.
On November 1, 2022, Cao Peng, Xie Zhiyong, Wang Fengchao and Shang Congping of Guangzhou National Laboratory of Beijing Institute of Biological Sciences published a research paper entitled "The gut-to-brain axis for toxin-induced defensive responses" online at Cell The study developed a mouse-based paradigm to study bacterial toxin-induced defense responses
.
Using this paradigm, the study identified a set of molecularly defined visceral to the brain and brain circuits that work together to mediate toxin-induced defense responses
.
The enterobrain gyrus consists of a group of Htr3a+ vagus nerve sensory neurons that transmit toxin-related signals from intestinal pheochromaffin cells to Tac1⁺ neurons in the dorsal vagal complex (DVC).

Tac1⁺ DVC neurons drive retching behavior and conditioned taste avoidance
through divergent projections to the rostral ventral respiratory group (rVRG) and lateral parabrachial nucleus, respectively.
Manipulating these circuits can also interfere with the defense response
caused by the chemotherapy drug doxorubicin.
Together, these results suggest that food poisoning and chemotherapy summon similar neural circuit modules to initiate a defensive response
.
In addition, on January 3, 2022, Cao Peng of Beijing Institute of Biological Sciences and Zhang Fan of Hebei Medical University jointly published a joint newsletter in Nature Neuroscience online entitled " Mechanically evoked defensive attack is controlled by GABAergic neurons in the anterior hypothalamic nucleus", which shows that harmful mechanical forces in an unavoidable environment are key stimuli
that trigger defensive aggression in laboratory mice.
Mechanically induced defensive attacks
can be eliminated by photosuppression of vGAT⁺ neurons in the anterior hypothalamic nucleus (AHN).
vGAT⁺AHN neurons encode the strength of mechanical forces and are innervated
by brain regions associated with pain and attack.
The activation of these neurons triggers a biting attack on the predator while inhibiting ongoing behavior
.
Projections from vGAT⁺AHN neurons to the gray matter surrounding the aqueduct may be an AHN pathway
involved in mechanically induced defensive attacks.
Together, these data suggest that vGAT⁺AHN neurons encode noxious mechanical stimuli and modulate defensive aggression in mice (click to read).

Once food contaminated with bacterial toxins is ingested, the brain initiates a cascade of defensive responses
.
These reactions include motor reflexes such as retching and vomiting, which promote the excretion of toxins from the gastrointestinal tract, and an unpleasant sensation known as "nausea," which acts as a signal that the condition avoids taste to prevent future ingestion of the same toxin
.
Paradoxically, these defensive responses, which protect the body from toxins, are the main cause of serious side effects of
chemotherapy drugs.
Over the past few decades, the neurobiology of toxin-induced defense responses has been studied
in depth.
By using animal models with the ability to vomit, studies have shown that the gut-to-brain axis is associated with
toxin-induced nausea and vomiting.
To support this hypothesis, the researchers found that the chemotherapy drugs cisplatin and enterotoxin induce the expression of Fos in the solitary tract nucleus (NTS), a brain region
innervated by vagus afferent nerves.
Vagus neurotomy eliminates vomiting
caused by cisplatin and enterotoxin.
Pharmacological studies have shown that antagonists of serotonin-3 receptors (5-HT3R) and neurokinin 1 receptors (NK1R) block cisplatin and enterotoxin-induced vomiting
.
However, this visceral-to-brain axis mechanism remains elusive, and there are some important questions to be answered
.
First, key neuronal isotypes in NTS and their efferent circuits that coordinate toxin-induced defense responses remain unmapped
.
Second, on this visceral-brain axis, the molecular and physiological properties of vagus sensory neurons are largely unknown
.
Third, little is known about cellular processes in the gut that are critical to toxin-induced defense
responses.
These questions are difficult to answer because the traditional experimental paradigm of toxin-induced defense responses is largely based on emetic species
.
Laboratory mice are rarely used for this type of study because they do not respond to vomiting with
emetics.
However, mice did exhibit conditioned taste avoidance (CFA) and potential retching-like behavior
.
In this study, a mouse-based experimental paradigm was developed, thus solving the above three questions
about the visceral-brain axis of toxin-induced defense responses in mice.
The study developed a mouse-based paradigm to study bacterial toxin-induced defense responses
.
Using this paradigm, the study identified a set of molecularly defined visceral to the brain and brain circuits that work together to mediate toxin-induced defense responses
.
The enterocerebral gyrus consists of a group of Htr3a+ vagus nerve sensory neurons that transmit toxin-related signals from intestinal pheochromaffin cells to Tac 1⁺ neurons in the dorsal vagal complex (DVC).

。 Tac1⁺ DVC neurons pass through the rostral Ventral Respiratory Group (rVRG) on the coracoid side of the bulbous spine, respectively and divergent projections of the lateral parabrachial nucleus drive retching behavior and conditioned taste avoidance
.
Manipulating these circuits can also interfere with the defense response
caused by the chemotherapy drug doxorubicin.
Together, these results suggest that food poisoning and chemotherapy summon similar neural circuit modules to initiate a defensive response
.

Reference Message:

https://doi.
org/10.
1016/j.
cell.
2022.
10.
001

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