ArticleThe Journal of physiology2004
Cyclooxygenase-2 contributes to dysmotility and enhanced excitability of myenteric AH neurones in the inflamed guinea pig distal colon.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 101 citations in OpenAlex.
- Obesity-Related Oxidative Stress and Antioxidant Properties of Natural Compounds in the Enteric Nervous System: A Literature Overview.Antioxidants (Basel, Switzerland) · 2026Review
- The Physiology of Enteric Glia.Annual review of physiology · 2025Review
- Enteric glia promote visceral hypersensitivity during inflammation through intercellular signaling with gut nociceptors.Science signaling · 2023Article
- The enteric nervous system.Physiological reviews · 2023Review
- Crosstalk between omega-6 oxylipins and the enteric nervous system: Implications for gut disorders?Frontiers in medicine · 2023Review
- The α isoform of cGMP-dependent protein kinase 1 (PKG1α) is expressed and functionally important in intrinsic primary afferent neurons of the guinea pig enteric nervous system.Neurogastroenterology and motility · 2021Article
- Functional circuits and signal processing in the enteric nervous system.Cellular and molecular life sciences : CMLS · 2020Review
- The effect of probiotics on ıntestinal motility in an experimental short bowel model.Acta cirurgica brasileira · 2020Article
- Enteric neuroplasticity and dysmotility in inflammatory disease: key players and possible therapeutic targets.American journal of physiology. Gastrointestinal and liver physiology · 2019Review
- Protective Actions of Epithelial 5-Hydroxytryptamine 4 Receptors in Normal and Inflamed Colon.Gastroenterology · 2016Article
- Enteric Neuronal Regulation of Intestinal Inflammation.Trends in neurosciences · 2016Review
- Auricular vagal nerve stimulation ameliorates burn-induced gastric dysmotility via sympathetic-COX-2 pathways in rats.Neurogastroenterology and motility · 2016Article
- Colitis-induced neuroplasticity disrupts motility in the inflamed and post-inflamed colon.The Journal of clinical investigation · 2015Review
- Colon distention induces persistent visceral hypersensitivity by mechanotranscription of pain mediators in colonic smooth muscle cells.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Neuroprotective Potential of Mesenchymal Stem Cell-Based Therapy in Acute Stages of TNBS-Induced Colitis in Guinea-Pigs.PloS one · 2015Article
- Experimental model of tympanic colic (acute abdomen) in chinchillas (Chinchilla lanigera).Laboratory animal research · 2014Article
- Mechanical stress is a pro-inflammatory stimulus in the gut: in vitro, in vivo and ex vivo evidence.PloS one · 2014Article
- Insights from a novel model of slow-transit constipation generated by partial outlet obstruction in the murine large intestine.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Neuronal activation and plasticity in Schistosoma mansoni infected mice.Saudi journal of biological sciences · 2012Article
- Mechano-transcription of COX-2 is a common response to lumen dilation of the rat gastrointestinal tract.Neurogastroenterology and motility · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
We have previously demonstrated that trinitrobenzene sulphonic acid (TNBS)-induced colitis in guinea pig is associated with hyperexcitability of myenteric AH neurones, enhanced synaptic activity in the myenteric plexus, increased serotonin (5-HT) availability in the mucosa, and decreased propulsive motor activity. The current study tested the hypothesis that the activation of cyclooxygenase (COX) contributes to these alterations in bowel functions. DFU inhibition of COX-2, but not SC-560 inhibition of COX-1, restored to normal levels the electrical properties of myenteric AH neurones, the proportion of S neurones exhibiting slow EPSPs, and the rate of propulsive motor activity. Neither inhibitor was effective in altering the level of inflammation, the increased availability of mucosal 5-HT, or the enhanced fast EPSPs in myenteric AH and S neurones. COX-2 expression is enhanced in the myenteric plexus and cells within the smooth muscle layers during colitis, possibly reflecting the site at which COX-2 inhibition acts to allow recovery of motor function. In support of this concept, COX-1, but not COX-2, inhibition was effective in restoring normal mucosal prostaglandin levels. These results indicate that the various changes that occur in the motor neural pathways of the distal colon in TNBS-induced colitis do not involve a single neuroimmune mechanism. COX-2 activation is a critical step in the enhanced excitability of AH neurones as well as diminished propulsive motility in TNBS colitis, whereas other yet to be resolved pathways, that do not involve COX-1 or COX-2 activation, lead to altered 5-HT content in the mucosa and an augmentation of fast EPSPs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.