Brain-gut Regulation
Brain-gut Regulation - Related Videos
01:22
Gut-Brain Axis
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2026
The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such as...
14:04
Brain Imaging Investigation of the Neural Correlates of Emotion Regulation
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Cited by 6 •
2011
We present a protocol that allows investigation of the neural correlates of deliberate and automatic emotion regulation, using functional magnetic resonance imaging. This protocol can be used in healthy participants, both young and older, as well as in clinical patients.
15:27
Extracting DNA from the Gut Microbes of the Termite (Zootermopsis Angusticollis) and Visualizing Gut Microbes
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Cited by 18 •
2007
This video illustrates the technique for extracting DNA from the species of microbes resident in the termite hindgut. The preparation of a wet mount slide, which is useful for visualizing the gut microbial community is also illustrated, and a tour through the species-rich gut environment is given.
01:55
Intracranial Injection of Gut-Derived Microbial Metabolites in a Mouse Model
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2025
Source: Liou, C. et al. Intracerebroventricular Delivery of Gut-Derived Microbial Metabolites in Freely Moving Mice. J. Vis. Exp. (2022).This video demonstrates the intracranial injection of short-chain fatty acids (SCFAs) in a freely moving mouse to study their effects on brain-mediated behavior. An injector cannula is inserted into a guide cannula implanted in the mouse brain. After recovery, the mouse acclimates in a novel cage. SCFAs are then administered, and locomotor behavior is recorded.
01:15
Assessing the Role of Gut Microbiota in Modulating Hepatitis B Infection in Mice
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2026
Take a control mouse with a normal gut microbiota and an experimental mouse with depleted gut microbiota. The depletion compromises the integrity of the gut barrier.This enables bacteria to translocate through the blood vessel into the liver tissue.Inject both mice with the hepatitis B virus or HBV plasmid to induce an HBV infection in the liver tissue.In the control mouse, the T cell detects an infected liver cell through the interaction of its receptors with viral antigens, and produces...
FAQs
Vagal signaling provides one neural route by which gastrointestinal activity can communicate with the brain and by which brain-related signals can influence gut function. This pathway operates alongside endocrine, immune, and microbial communication rather than acting alone. Considering these channels together helps explain why digestive changes may coincide with alterations in mood, stress responses, or symptom perception.
Stress-hormone circuits can modify gastrointestinal motility, meaning the movement of contents through the digestive tract, and can also change gut sensitivity. These effects help connect psychological stress with symptoms that may not be explained solely by local digestive activity. In medical research, separating altered movement from heightened sensitivity can clarify how stress contributes to functional gastrointestinal disorders.
Intestinal microorganisms contribute chemical signals that participate in brain-gut communication. Along with inflammatory mediators, these signals provide a route through which changes in the gastrointestinal environment may influence behavior and cognition. This mechanism broadens investigation beyond nerves and hormones, supporting research into how microbial or inflammatory changes might relate to brain-associated symptoms.
These pathways differ in the type of information they convey and in how they may affect the system. Neural signaling includes vagal communication, endocrine signaling includes stress-hormone circuits, and immune signaling includes inflammatory mediators. Examining them in combination is more informative than attributing every brain-gut effect to a single mechanism, particularly when studying complex medical conditions.
Brain-gut regulation is especially relevant to irritable bowel syndrome and functional gastrointestinal disorders because stress-related changes in motility or sensitivity may contribute to symptoms. It also informs research on inflammatory bowel disease, where gastrointestinal inflammation is part of the clinical context. The framework encourages attention to interacting neural, stress, immune, and microbial factors rather than one isolated cause.
The framework supports approaches aimed at stress pathways, diet, the microbiome, or neural communication. These targets represent different entry points into the same interconnected system rather than interchangeable therapies. Studying them may help investigators determine whether changing psychological, gastrointestinal, microbial, or neural factors alters digestive activity, mood, stress responses, or related symptoms.
Changes in the gastrointestinal tract can be studied not only for digestive consequences but also for possible effects on behavior and cognition. Conversely, psychological stress can be examined as a factor that changes gut motility and sensitivity. This two-way perspective encourages medical research to track gastrointestinal and brain-related outcomes together rather than treating them as unrelated problems.