ArticleThe Journal of physiology2013
Oxidative stress disrupts purinergic neuromuscular transmission in the inflamed colon.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Role of mitochondria in neuronal function and survival in the enteric and central nervous systems.Cellular and molecular life sciences : CMLS · 2026Review
- The Oxidative Stress and Nervous Distress Connection in Gastrointestinal Disorders.Biomolecules · 2023Review
- Oxidative Stress-Induced HMGB1 Translocation in Myenteric Neurons Contributes to Neuropathy in Colitis.Biomolecules · 2022Article
- LPAR1 regulates enteric nervous system function through glial signaling and contributes to chronic intestinal pseudo-obstruction.The Journal of clinical investigation · 2022Article
- Neurotransmitters responsible for purinergic motor neurotransmission and regulation of GI motility.Autonomic neuroscience : basic & clinical · 2021Article
- Enteric glial biology, intercellular signalling and roles in gastrointestinal disease.Nature reviews. Gastroenterology & hepatology · 2021Review
- Etiology of Colitis-Complex Diarrhea in Growing Pigs: A Review.Animals : an open access journal from MDPI · 2021Review
- Inhibition of APE1/Ref-1 Redox Signaling Alleviates Intestinal Dysfunction and Damage to Myenteric Neurons in a Mouse Model of Spontaneous Chronic Colitis.Inflammatory bowel diseases · 2021Article
- Diminished enteric neuromuscular transmission in the distal colon following experimental spinal cord injury.Experimental neurology · 2020Article
- Recommendations for evaluation of bladder and bowel function in pre-clinical spinal cord injury research.The journal of spinal cord medicine · 2020Review
- The nitroxide 4-methoxy-tempo inhibits the pathogenesis of dextran sodium sulfate-stimulated experimental colitis.Redox biology · 2020Article
- Enteric neuroplasticity and dysmotility in inflammatory disease: key players and possible therapeutic targets.American journal of physiology. Gastrointestinal and liver physiology · 2019Review
- NTPDase1 and -2 are expressed by distinct cellular compartments in the mouse colon and differentially impact colonic physiology and function after DSS colitis.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Intestinal nerve cell injury occurs prior to insulin resistance in female mice ingesting a high-fat diet.Cell and tissue research · 2019Article
- Anatomical and Functional Changes to the Colonic Neuromuscular Compartment after Experimental Spinal Cord Injury.Journal of neurotrauma · 2018Article
- Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease.World journal of gastroenterology · 2017Review
- Role of oxidative stress in oxaliplatin-induced enteric neuropathy and colonic dysmotility in mice.British journal of pharmacology · 2016Article
- 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
- Fundamentals of Neurogastroenterology: Basic Science.Gastroenterology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Colitis, induced by trinitrobenzene sulfonic acid (TNBS) in guinea pig, leads to decreased purinergic neuromuscular transmission resulting in a reduction in inhibitory junction potentials (IJPs) in colonic circular muscle. We explored possible mechanisms responsible for this inflammation-induced neurotransmitter plasticity. Previous studies have suggested that the deficit in inflamed tissue involves decreased ATP release. We therefore hypothesized that decreased purinergic transmission results from inflammation-induced free radical damage to mitochondria, leading to decreased purine synthesis and release. Stimulus-induced release of purines was measured using high-performance liquid chromatography, and quantities of all purines measured were significantly reduced in the inflamed colons as compared to controls. To test whether decreased mitochondrial function affects the IJP, colonic muscularis preparations were treated with the mitochondrial ATP synthase inhibitors oligomycin or dicyclohexylcarbodiimide, which resulted in a significant reduction of IJP amplitude. Induction of oxidative stress in vitro, by addition of H2O2 to the preparation, also significantly reduced IJP amplitude. Purinergic neuromuscular transmission was significantly restored in TNBS-inflamed guinea pigs, and in dextran sodium sulfate-inflamed mice, treated with a free radical scavenger. Furthermore, propulsive motility in the distal colons of guinea pigs with TNBS colitis was improved by in vivo treatment with the free radical scavenger. We conclude that oxidative stress contributes to the reduction in purinergic neuromuscular transmission measured in animal models of colitis, and that these changes can be prevented by treatment with a free radical scavenger, resulting in improved motility.
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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.