ArticleThe journal of physiological sciences : JPS2013
Alteration of neuromuscular transmissions in the hamster colon following the resolution of TNBS-induced colitis.
Article in The journal of physiological sciences : JPS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Possible Involvement of Descending Monoaminergic Pathways in Colorectal Dysmotility Using a Rat Model of Colitis.Neurogastroenterology and motility · 2026Article
- Interaction between the Renin-Angiotensin System and Enteric Neurotransmission Contributes to Colonic Dysmotility in the TNBS-Induced Model of Colitis.International journal of molecular sciences · 2021Article
- Local regulatory mechanism to coordinate colorectal motility in rats.Physiological reports · 2018Article
- Actions of probiotics on trinitrobenzenesulfonic acid-induced colitis in rats.BioMed research international · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
The aim of this study was to determine whether trinitrobenzene sulfonic acid-induced colitis leads to alterations in enteric neuronal transmission in hamsters. We assessed the mechanical responses induced by the application of electrical field stimulation (EFS) in isolated segments of the distal colon. The EFS-induced relaxation and contraction were blocked by a nitric oxide synthase inhibitor and by the combination of antagonists for tachykinin NK1 and NK2 receptors and muscarinic acetylcholine receptors, respectively. The mechanical responses to EFS were attenuated in the inflamed colon at 7 days and were recovered by 30 days after inflammation treatment. In addition, we found that purinergic and opioidergic excitatory neural components are expressed following the resolution of colitis. These results suggest that colonic inflammation causes indiscriminate damage to enteric neurons but that neuronal components are restored and that new excitatory neural components, compensating for the contractile responses in smooth muscle after colitis, are expressed.
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Registered trials
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