ArticlePain2008
Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach-brainstem axis.
Article in Pain, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- The association between dietary acid load and odds and severity of irritable bowel syndrome in adults.Scientific reports · 2022Article
- pH and proton-sensitive receptors in brain ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Article
- Pathology and physiology of acid‑sensitive ion channels in the digestive system (Review).International journal of molecular medicine · 2022Review
- Acid-sensing ion channel 3: An analgesic target.Channels (Austin, Tex.) · 2021Review
- Upregulation of the TRPA1 Ion Channel in the Gastric Mucosa after Iodoacetamide-Induced Gastritis in Rats: A Potential New Therapeutic Target.International journal of molecular sciences · 2020Article
- Review
- Distinct Expression of Phenotypic Markers in Placodes- and Neural Crest-Derived Afferent Neurons Innervating the Rat Stomach.Digestive diseases and sciences · 2018Article
- Pharmacological evaluation of NSAID-induced gastropathy as a "Translatable" model of referred visceral hypersensitivity.World journal of gastroenterology · 2017Article
- Pharmacological Approach for Managing Pain in Irritable Bowel Syndrome: A Review Article.Anesthesiology and pain medicine · 2017Review
- Endogenous Isoquinoline Alkaloids Agonists of Acid-Sensing Ion Channel Type 3.Frontiers in molecular neuroscience · 2017Article
- Acid-Sensing Ion Channels as Potential Therapeutic Targets in Neurodegeneration and Neuroinflammation.Mediators of inflammation · 2017Review
- Non-acidic activation of pain-related Acid-Sensing Ion Channel 3 by lipids.The EMBO journal · 2016Article
- Acid-sensing ion channels in gastrointestinal function.Neuropharmacology · 2015Review
- Antinociceptive effects of amiloride and benzamil in neuropathic pain model rats.Journal of Korean medical science · 2013Article
- Environmental enrichment and gut inflammation modify stress-induced c-Fos expression in the mouse corticolimbic system.PloS one · 2013Article
- Human ASIC3 channel dynamically adapts its activity to sense the extracellular pH in both acidic and alkaline directions.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Asic3 is a neuronal mechanosensor for pressure-induced vasodilation that protects against pressure ulcers.Nature medicine · 2012Article
- ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012Review
- Drug management of visceral pain: concepts from basic research.Pain research and treatment · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Gastric acid challenge of the rat and mouse stomach is signalled to the brainstem as revealed by expression of c-Fos. The molecular sensors relevant to the detection of gastric mucosal acidosis are not known. Since the acid-sensing ion channels ASIC2 and ASIC3 are expressed by primary afferent neurons, we examined whether knockout of the ASIC2 or ASIC3 gene modifies afferent signalling of a gastric acid insult in the normal and inflamed stomach. The stomach of conscious mice (C57BL/6) was challenged with intragastric HCl; two hours later the activation of neurons in the nucleus tractus solitarii (NTS) of the brainstem was visualized by c-Fos immunocytochemistry. Mild gastritis was induced by addition of iodoacetamide (0.1%) to the drinking water for 7 days. Exposure of the gastric mucosa to HCl (0.25M) caused a 3-fold increase in the number of c-Fos-positive neurons in the NTS. This afferent input to the NTS remained unchanged by ASIC3 knockout, whereas ASIC2 knockout augmented the c-Fos response to gastric HCl challenge by 33% (P<0.01). Pretreatment of wild-type mice with iodoacetamide induced mild gastritis, as revealed by increased myeloperoxidase activity, and enhanced the number of NTS neurons responding to gastric HCl challenge by 41% (P<0.01). This gastric acid hyperresponsiveness was absent in ASIC3 knockout mice but fully preserved in ASIC2 knockout mice. The current data indicate that ASIC3 plays a major role in the acid hyperresponsiveness associated with experimental gastritis. In contrast, ASIC2 appears to dampen acid-evoked input from the stomach to the NTS.
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