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Repeated psychological stress is associated with symptoms similar to irritable bowel syndrome

Repeated psychological stress is associated with symptoms similar to irritable bowel syndrome

Summary: Chronic stress induces symptoms similar to irritable bowel syndrome in mouse models.

Source: Tokyo University of Science

Irritable bowel syndrome (IBS) often presents with gastrointestinal symptoms in the small and large intestines. IBS is categorized into four subtypes depending on stool inconsistency; these are IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), mixed (IBS-M) and unclassified IBS. But there is a lack of understanding in the scientific literature about the mechanisms and treatments of IBS. One reason for this lack of knowledge about IBS is the lack of useful experimental animal models.

Over the years, studies have suggested a link between emotional states and gut dysfunction, highlighting the existence and importance of the so-called “gut-brain axis” in determining our emotional and metabolic well-being.

Recently, chronic social defeat stress (cSDS) and chronic social defeat stress (cVSDS) have been accepted as models for major depressive disorder (MDD) and posttraumatic stress disorder.

Can cVSDS animal models help us understand IBS in detail? To find out, researchers at Tokyo University of Science (TUS) led by Professor Akiyoshi Saitoh of the Faculty of Pharmaceutical Sciences, TUS, used cVSDS mouse models. Their goal was to understand the effects of long-term psychological stress on intestinal conditions.

The team found that mice exposed to psychological stress exhibited a higher ratio of intestinal transit to visceral pain-related behaviors – hallmarks of IBS.

Their findings were published in Frontiers in Neuroscience.

Elaborating his study, prof. Says Saitoh, “we focused on the cVSDS paradigm and assessed the impact of emotional stress on gut conditions. We further evaluated the potential of the paradigm as a new animal model of IBS.”

In their study, they subjected mice to physical stress or emotional stress, in which the test animals either underwent physical aggression or witnessed aggression for 10 minutes a day for 10 consecutive days.

On day 11, a social interaction test was conducted to assess the stress conditions of the test animals. Stress was also assessed by quantification of plasma corticosterone, the charcoal meal test, and the capsaicin-induced hyperalgesia test in animals. The researchers also evaluated the mice for intestinal permeability, pathology, defecation frequency and stool content.

They found that the charcoal transit ratio, which indicates passage through the gut, was significantly elevated in mice subjected to emotional stress compared to mice in a control (naïve) group that was not exposed to stress. However, the effects were insignificant in mice subjected to physical stress. Defecation frequency and stool water content were also increased in mice subjected to emotional stress.

These effects lasted for 1 month after the stress load. In addition, there were no significant differences in pathological status and intestinal permeability between naïve and emotionally stressed mice, indicating no tissue-level changes due to stress.

This shows a man holding his stomach
Over the years, studies have suggested a link between emotional states and gut dysfunction, highlighting the existence and importance of the so-called “gut-brain axis” in determining our emotional and metabolic well-being. Image is in the public domain

Professor Saitoh says: “These results suggest that chronic stress in mice induces IBS-D-like symptoms, such as chronic intestinal peristaltic exacerbations and abdominal hyperalgesia, without intestinal lesions.”

Interestingly, the researchers found that changes in intestinal motility in the test animals were improved when the cVSDS mice were treated with keishikashakuyakuto, a campo drug used clinically to treat IBS.

The study highlights the advantage of the cVSDS paradigm over traditional methods in inducing IBS-D-like symptoms through exposure to repeated psychological stress.

Speaking about the mechanisms of these effects, Professor Saitoh says: “From the perspective of the gut-brain axis, we suspect that the insular cortex plays an important role in determining the emotionally stressed phenotype of mice.” The insular cortex is part of the upper central nervous system that controls digestive functions and is involved in the process of dealing with psychological stress.

In conclusion, this study demonstrates for the first time that cVSDS-induced psychological stress alone can cause IBS-D-like symptoms in mice. Further research could perhaps rely on the cSDS and cVSDS paradigms to elucidate the pathophysiological conditions and design treatments for IBS.

About this news about stress research

Author: Press Office
Source: Tokyo University of Science
Contact: Press Office – Tokyo University of Science
picture: Image is in the public domain

Original Research: Open access.
Repeated psychological stress, chronic social defeat stress, induces symptoms similar to irritable bowel syndrome in mice” Toshinori Yoshioka et al. Frontiers in Neuroscience

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Abstract

Repeated psychological stress, chronic social defeat stress, induces symptoms similar to irritable bowel syndrome in mice

A growing body of evidence shows that emotional states and gut states are interconnected in so-called “brain-gut interactions.” Indeed, many psychiatric disorders are accompanied by gastrointestinal symptoms, such as irritable bowel syndrome (IBS).

However, a functional link remains elusive, in part because there are few useful experimental animal models.

Here, we focused on a highly validated animal model of stress-induced psychiatric disorders, such as depression, known as the chronic social defeat mouse model (cVSDS), which we prepared using exposure to repeated psychological stress, after which we examined their gut conditions. .

In the charcoal meal test and the capsaicin-induced hyperalgesia test, the cVSDS model mice showed a significantly higher intestinal transit ratio and increased visceral pain-related behavior, respectively. These changes persisted for more than a month after the stress session.

On the other hand, pathological evaluations of histological and inflammatory results of naïve and cVSDS mouse models did not differ. Furthermore, keishikashakuyakuto—a campo drug used clinically to treat IBS—normalized the change in intestinal motility in the cVSDS mouse model.

Our results show that cVSDS model mice exhibit IBS-like symptoms such as chronic intestinal peristaltic changes and abdominal hyperalgesia without organic lesions.

Therefore, we propose the cVSDS paradigm as a new animal model of IBS with broad validity, elucidating the correlation between depressive states and intestinal abnormalities.



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