ArticleProceedings of the National Academy of Sciences of the United States of America2011
T-type calcium channels contribute to colonic hypersensitivity in a rat model of irritable bowel syndrome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 146 citations in OpenAlex.
- Ethosuximide and Irritable Bowel Syndrome-Related Abdominal Pain: A Randomized Clinical Trial.JAMA network open · 2026Trial
- Trial
- Trial
- Functional expression of the T-type Cav3.2 calcium channel in female and male human dorsal root ganglion neurons.Brain : a journal of neurology · 2026Article
- Altered Sigmoid Mucosal Innervation and Mast Cell Proximity to Sensory Nerve Fibers Are Associated With Symptom Severity in Patients With Irritable Bowel Syndrome.Neurogastroenterology and motility · 2025Article
- A pathological missense mutation in the deubiquitinase USP5 leads to insensitivity to pain.The Journal of experimental medicine · 2025Article
- Gut sensory neurons as regulators of neuro-immune-microbial interactions: from molecular mechanisms to precision therapy for IBD/IBS.Journal of neuroinflammation · 2025Review
- Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025Review
- Review
- Piezo2 channels expressed by colon-innervating TRPV1-lineage neurons mediate visceral mechanical hypersensitivity.Neuron · 2023Article
- Involvement of acid sensing ion channel (ASIC)-3 in an acute urinary bladder-colon cross sensitization model in rodent.Frontiers in pain research (Lausanne, Switzerland) · 2023Article
- Distinctions Between Fecal and Intestinal Mucosal Microbiota in Subgroups of Irritable Bowel Syndrome.Digestive diseases and sciences · 2022Article
- Pathophysiology of Post-Traumatic Trigeminal Neuropathic Pain.Biomolecules · 2022Review
- Central and peripheral contributions of T-type calcium channels in pain.Molecular brain · 2022Review
- Voltage-dependent CaPflugers Archiv : European journal of physiology · 2022Review
- Small Molecules as Modulators of Voltage-Gated Calcium Channels in Neurological Disorders: State of the Art and Perspectives.Molecules (Basel, Switzerland) · 2022Review
- Design of 1,4-Dihydropyridine Hybrid Benzamide Derivatives: Synthesis and Evaluation of Analgesic Activity and Their Molecular Docking Studies.Drug design, development and therapy · 2022Article
- The Mechanisms of Plasticity of Nociceptive Ion Channels in Painful Diabetic Neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Mechanism of the Treatment of Irritable Bowel Syndrome with Sini Powder and Tong Xie Yao Fang Decoction Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- A Potential Role of Ethosuximide and Pentoxifylline in Relieving Abdominal Pain in Irritable Bowel Syndrome Patients Treated with Mebeverine: A Randomized, Double-Blind, Placebo-Controlled Trial.Journal of inflammation research · 2022Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The symptoms of irritable bowel syndrome (IBS) include significant abdominal pain and bloating. Current treatments are empirical and often poorly efficacious, and there is a need for the development of new and efficient analgesics aimed at IBS patients. T-type calcium channels have previously been validated as a potential target to treat certain neuropathic pain pathologies. Here we report that T-type calcium channels encoded by the Ca(V)3.2 isoform are expressed in colonic nociceptive primary afferent neurons and that they contribute to the exaggerated pain perception in a butyrate-mediated rodent model of IBS. Both the selective genetic inhibition of Ca(V)3.2 channels and pharmacological blockade with calcium channel antagonists attenuates IBS-like painful symptoms. Mechanistically, butyrate acts to promote the increased insertion of Ca(V)3.2 channels into primary sensory neuron membranes, likely via a posttranslational effect. The butyrate-mediated regulation can be recapitulated with recombinant Ca(V)3.2 channels expressed in HEK cells and may provide a convenient in vitro screening system for the identification of T-type channel blockers relevant to visceral pain. These results implicate T-type calcium channels in the pathophysiology of chronic visceral pain and suggest Ca(V)3.2 as a promising target for the development of efficient analgesics for the visceral discomfort and pain associated with IBS.
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