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Updated: Aug 11, 2026
In vitro Functional Characterization of Mouse Colorectal Afferent Endings
Published on: January 21, 2015
CB1 and TRPV1 receptors mediate protective effects on colonic electrophysiological properties in mice
1Department of Internal Medicine II and Institute of Surgical Research, Ludwig-Maximilians University Munich, Marchioninistr. 15, 81377, Munich, Germany.
Abstract:
CB1 and TRPV1 receptors modulate enteric neurotransmission and colonic inflammation. This study investigates early electrophysiological changes in distal colon of wild-type and receptor deficient mice after an inflammatory insult set by dinitrobenzene sulfonic acid (DNBS). Colitis was induced by DNBS in CB1(-/-) mice, TRPV1(-/-) mice, and their respective wild-type littermates. Electrophysiological properties consisting of membrane potentials and electrically induced inhibitory junction potentials (IJP) of circular smooth muscle cells were evaluated at different time points. Additionally a histological colitis severity score was evaluated in CB1(+/+) and CB1(-/-) mice 24 h after DNBS. Inflammation caused spontaneous atropine insensitive rhythmic action potentials in CB1(-/-) and TRPV1(-/-) mice but not in wild-type animals. This indicates that membrane stability is disturbed, which in turn indicates a lack of protective mechanisms. Focal electrical neuronal stimulation of the myenteric plexus induced IJP in the smooth muscle cells. Twenty-four hours after initiation of inflammation, the duration of the IJP is prolonged in all animals, indicating disturbances within neuromuscular interaction. In CB1(-/-) mice, it is interesting that the duration of IJP was significantly extended, as compared to CB1(+/+) mice pointing toward missing protective mechanisms in the CB1(-/-) mice. Inflammatory insults in the mouse colon induce reproducible changes in the electrophysiological properties and such changes correlate with duration of colitis. In mutants, these electrophysiological changes display different patterns, suggesting the lack of protective properties for neuromuscular interactions and membrane stability.
Insights
Inflammation disrupts colon electrical activity in mice lacking CB1 or TRPV1 receptors, indicating a loss of protective mechanisms. These changes highlight receptor roles in maintaining gut stability during colitis.
Area of Science:
- Gastroenterology
- Neuroscience
- Physiology
Background:
- Cannabinoid receptor 1 (CB1) and transient receptor potential vanilloid 1 (TRPV1) receptors influence gut function and inflammation.
- Enteric neurotransmission and colonic inflammation are modulated by CB1 and TRPV1 signaling pathways.
Purpose of the Study:
- To investigate early electrophysiological alterations in the distal colon of mice deficient in CB1 or TRPV1 receptors following dinitrobenzene sulfonic acid (DNBS)-induced colitis.
- To assess the role of CB1 and TRPV1 receptors in maintaining colonic membrane stability and neuromuscular function during inflammation.
Main Methods:
- Induction of colitis using DNBS in wild-type, CB1(-/-), and TRPV1(-/-) mice.
- Evaluation of circular smooth muscle cell membrane potentials and inhibitory junction potentials (IJP) at various time points post-DNBS.
- Histological assessment of colitis severity in CB1(+/+) and CB1(-/-) mice.
Main Results:
- DNBS-induced inflammation triggered spontaneous action potentials in CB1(-/-) and TRPV1(-/-) mice, but not wild-type, suggesting compromised membrane stability.
- A prolonged IJP duration was observed in all groups 24 hours after DNBS, indicating neuromuscular disturbances.
- CB1(-/-) mice exhibited a significantly longer IJP duration compared to wild-type, pointing to a lack of protective mechanisms.
Conclusions:
- Colonic inflammation induces reproducible electrophysiological changes that correlate with colitis severity.
- Receptor-deficient mice display distinct electrophysiological patterns, highlighting the protective roles of CB1 and TRPV1 in neuromuscular interactions and membrane stability during colitis.
