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Updated: May 19, 2026

In vitro Functional Characterization of Mouse Colorectal Afferent Endings
Published on: January 21, 2015
Luminal hypertonicity and acidity modulate colorectal afferents and induce persistent visceral hypersensitivity
Jun-Ho La1, Bin Feng, Erica S Schwartz
1Center for Pain Research, Department of Anesthesiology, School of Medicine, University of Pittsburgh, W1402 Biomedical Science Tower, 200 Lothrop St. Pittsburgh, PA 15213, USA. laj@upmc.edu
Carbohydrate malabsorption causes abdominal pain by increasing colon acidity and hypertonicity. These factors alter colorectal sensory nerves, leading to hypersensitivity and pain, as shown in mouse models.
Area of Science:
- Gastroenterology
- Neuroscience
- Pain Research
Background:
- Carbohydrate malabsorption, common in lactose intolerance and infections, leads to abdominal pain.
- This occurs due to increased intracolonic osmolarity and acidity from undigested carbohydrates.
Purpose of the Study:
- To investigate if hypertonicity and acidity modulate colorectal afferents.
- To determine the association between these factors and colorectal nociception/hypersensitivity.
Main Methods:
- In vitro mouse colorectum-pelvic nerve preparations to monitor afferent activity.
- Intracolonic instillation of acidic hypertonic saline (AHS) in mice.
- Behavioral assessment of colorectal distension (CRD) response and neuronal activation marker (pERK) expression.
Main Results:
- AHS excited 80% of serosal and 42% of mechanically-insensitive colorectal afferents (MIAs) in vitro.
- Intracolonic AHS increased pERK expression and augmented noxious CRD responses.
- Repeated AHS treatment induced long-lasting hypersensitivity to CRD and altered afferent proportions.
Conclusions:
- Luminal hypertonicity and acidity, resulting from carbohydrate malabsorption, can induce colorectal hypersensitivity.
- These factors alter colorectal afferent excitability and proportions, potentially contributing to abdominal pain.
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