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Long-term exercise can reduce the risk ofchronic diseases such as high blood pressure and diabetes.
Recent studies have shown that blood transfusion from regular exercise mice into aging mice significantly promotes hippocampal nerve regeneration
.
For some people, exercise is rewarding, promoting more and longer-term exercise activities
.
On December 14, 2022, Christoph A.
Thaiss's team at the University of Pennsylvania's Perelman School of Medicine revealed the intrinsic mechanism by which the body drives motor motivation: gut-brain axis signaling regulates motor behavior
by promoting the release of striatal dopamine.
1
Intestinal flora regulates motility in mice
The researchers trained 199 diverse off-line propagated mice from 8 identified strains and found that genes had littleeffect on the exercise capacity of mice through genomic analysis.
Exercise trained mice had reduced motor skills after receiving antibiotic treatment, and transplantation of exercise trained mouse gut flora into germ-free mice enhanced their exercise capacity
.
Figure 1: Reduced motor skills in mice after antibiotic treatment
2
Striatal dopamine drives mouse locomotion
The striatum is a key brain regionthat drives motivational behavior.
After exercise training, striatal neuronal activity increases, dopamine release increases, and exercise after the elimination of intestinal microorganisms with antibiotics does not activate striatal neurons and does not promote dopamine release
.
Activation of dopamine receptors by dopamine agonists reverses antibiotic-induced decline in exercise capacity
.
In addition, dopamine receptor antagonists inhibiting dopamine receptors or chronic inhibition of dopamine neuronal activity in the VTA region through chemogenetics can cause a weakening of motor capacity in mice, simulating the behavioral effect
of antibiotics.
Monoamine oxidase (MAO) mediates the degradation of dopamine, and MAO expression decreases
in the striatum of mice after exercise training.
Inhibition of MAO activity reverses antibiotic-induced loss of exercise capacity
.
3
Intestinal secretion and metabolism activate sensory neurons to regulate motor ability
The gut can transmit signals to thebrain through microbial metabolites or afferent neuronal circuits.
Most spinal cord and vagus afferent neurons express the ion channel receptor TRPV1, and the researchers found that the mice had impaired exercise ability after destroying TRPV1-positive sensory neurons or inhibiting their activity
.
Low-dose TRPV1 agonists significantly improve antibiotic-induced exercise dysfunction
.
In addition, exercise training activates sensory neurons in the dorsal root ganglion region, and antibiotic treatment reduces the activation of neurons in this area, suggesting that spinal TRPV1-positive sensory neurons sense signals from gut microbial origin
.
The researchers further discovered through metabolomics techniques the microbial metabolites that activate sensory neurons in the dorsal root ganglion region, fatty acid amides (FAAs
).
Mice were able to effectively alleviate antibiotic-induced exercise dysfunction
after ingesting FAAs.
Some metabolites of FAAs have been shown to act as agonists
of endocannabinoid CB1 receptors.
TRPV1-positive sensory neurons in the dorsal root ganglion region are enriched to express CB1, and in knockout CB1 mice, exercise does not activate TRPV1-positive sensory neurons and does not promote the release
of striatal dopamine.
Peripheral CB1 receptor antagonists inhibit motility in mice and regain motility after activating striatal dopamine
signaling.
In addition, CB1 receptor agonists promoted locomotility
in mice.
Figure 3: The intestinal metabolite FAA promotes exercise capacity in mice
summary
This article reveals that the intestinal flora activates peripheral TRPV1-positive sensory neurons, promotes the release of striatal dopamine, and enhances the motivational behavior
of exercise by producing fatty acid amides and other substances.
【References】
1.
https://doi.
org/10.
1038/s41586-022-05525-z
The images in the article are from references
