ArticleMolecular pain2013
Role of voltage gated Ca2+ channels in rat visceral hypersensitivity change induced by 2,4,6-trinitrobenzene sulfonic acid.
Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Mechanistic Insights into a Self-Management Intervention in Young Adults with Irritable Bowel Syndrome: A Pilot Multi-Omics Study.Biomedicines · 2025Article
- CCR2 Regulates Referred Somatic Hyperalgesia by Mediating T-Type CaBrain sciences · 2025Article
- A Multitrait Analysis of Genome-Wide Association Study Reveals the Shared Genetic Architecture Between Inflammatory Bowel Disease and Ankylosing Spondylitis.Mediators of inflammation · 2025Article
- Role of Cav2.3 (R-type) Calcium Channel in Pain and Analgesia: A Scoping Review.Current neuropharmacology · 2024Article
- Metformin inhibits spontaneous excitatory postsynaptic currents in spinal dorsal cord neurons from paclitaxel-treated rats.Frontiers in synaptic neuroscience · 2023Article
- cAMP signaling through protein kinase A and Epac2 induces substance P release in the rat spinal cord.Neuropharmacology · 2021Article
- Importance of Non-pharmacological Approaches for Treating Irritable Bowel Syndrome: Mechanisms and Clinical Relevance.Frontiers in pain research (Lausanne, Switzerland) · 2020Review
- Sleep deprivation of rats increases postsurgical expression and activity of L-type calcium channel in the dorsal root ganglion and slows recovery from postsurgical pain.Acta neuropathologica communications · 2019Article
- High-Voltage-Activated Calcium Channel in the Afferent Pain Pathway: An Important Target of Pain Therapies.Neuroscience bulletin · 2019Article
- Review
- Intracellular ion and protein nanoparticle-induced osmotic pressure modify astrocyte swelling and brain edema in response to glutamate stimuli.Redox biology · 2019Article
- Gene Network Dysregulation in the Trigeminal Ganglia and Nucleus Accumbens of a Model of Chronic Migraine-Associated Hyperalgesia.Frontiers in systems neuroscience · 2018Article
- Efficacy of otilonium bromide in irritable bowel syndrome: a pooled analysis.Therapeutic advances in gastroenterology · 2017Article
- A novel model for studying ileitis-induced visceral hypersensitivity in goats.Acta veterinaria Scandinavica · 2016Article
- Review: CaThe open neurology journal · 2016Article
- Colonic smooth muscle cells and colonic motility patterns as a target for irritable bowel syndrome therapy: mechanisms of action of otilonium bromide.Therapeutic advances in gastroenterology · 2014Review
- Differential Cav2.1 and Cav2.3 channel inhibition by baclofen and α-conotoxin Vc1.1 via GABAB receptor activation.The Journal of general physiology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVisceral pain is common symptom involved in many gastrointestinal disorders such as inflammatory bowel disease. The underlying molecular mechanisms remain elusive. We investigated the molecular mechanisms and the role for voltage gated calcium channel (VGCC) in the pathogenesis in a rat model of 2,4,6-trinitrobenzenesulfonic acid (TNBS) induced visceral inflammatory hypersensitivity.
resultsUsing Agilent cDNA arrays, we found 172 genes changed significantly in dorsal root ganglia (DRG) of TNBS treated rats. Among these changed genes, Cav1.2 and Cav2.3 were significantly up-regulated. Then the RT-PCR and Western blot further confirmed the up-regulation of Cav1.2 and Cav2.3. The whole cell patch clamp recording of acutely dissociated colonic specific DRG neurons showed that the peak IBa density was significantly increased in colonic neurons of TNBS treated rats compared with control rats (-127.82 ± 20.82 pA/pF Vs -91.67 ± 19.02 pA/pF, n = 9, *P < 0.05). To distinguish the different type of calcium currents with the corresponding selective channel blockers, we found that L-type (-38.56 ± 3.97 pA/pF Vs -25.75 ± 3.35 pA/pF, n = 9, * P < 0.05) and R-type (-13.31 ± 1.36 pA/pF Vs -8.60 ± 1.25 pA/pF, n = 9, * P < 0.05) calcium current density were significantly increased in colonic DRG neurons of TNBS treated rats compared with control rats. In addition, pharmacological blockade with L-type antagonist (nimodipine) and R-type antagonist (SNX-482) with intrathecal injection attenuates visceral pain in TNBS induced inflammatory visceral hypersensitivity.
conclusionCav1.2 and Cav2.3 in colonic primary sensory neurons play an important role in visceral inflammatory hyperalgesia, which maybe the potential therapeutic targets.
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