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Bladder-colon chronic cross-sensitization involves neuro-glial pathways in male mice
Karim Atmani1, Fabien Wuestenberghs1,2,3, Maximilien Baron1,4
1Nutrition, Gut and Brain Unit (Inserm U1073), Institute for Research and Innovation in Biomedicine, Université de Rouen Normandie, Rouen 76000, France.
World Journal of Gastroenterology
|January 12, 2023
Summary
This study introduces a new mouse model for bladder-colon cross-sensitization, revealing that acetic acid instillation causes long-term colorectal hypersensitivity. This hypersensitivity is driven by neuroglial interactions, MAPK-p38 activation, and NK1 receptors in the spinal cord.
Area of Science:
- Neuroscience
- Gastroenterology
- Urology
Background:
- Irritable bowel syndrome and bladder pain syndrome share symptoms like visceral hypersensitivity.
- Pelvic organs may experience cross-sensitization due to shared sensory pathways.
- The exact mechanisms behind bladder-colon cross-sensitization are not fully understood.
Purpose of the Study:
- To establish a mouse model for chronic bladder-colon cross-sensitization.
- To investigate the underlying mechanisms of this cross-sensitization.
Main Methods:
- Developed a model using ultrasound-guided intravesical acetic acid injections in mice.
- Assessed colorectal sensitivity via intracolonic pressure during distensions.
- Measured spinal cord c-Fos expression, microglia activation, NK1 receptor, and MAPK-p38 levels.
Main Results:
- Acetic acid induced hypersensitivity to colorectal distension lasting up to 7 days.
- Increased spinal cord c-Fos expression and microglia activation were observed.
- Elevated NK1 receptor and MAPK-p38 levels were detected in the spinal cord.
Conclusions:
- A novel model for bladder-colon cross-sensitization in mice was developed.
- Acetic acid instillation leads to sustained colorectal hypersensitivity.
- Neuroglial interactions, MAPK-p38 phosphorylation, and NK1 receptor signaling mediate this effect.
