ArticleExperimental neurology2007
Up-regulation of calcitonin gene-related peptide and receptor tyrosine kinase TrkB in rat bladder afferent neurons following TNBS colitis.
Article in Experimental neurology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization.The Journal of pharmacology and experimental therapeutics · 2024Review
- Plp1-expresssing perineuronal DRG cells facilitate colonic and somatic chronic mechanical pain involving Piezo2 upregulation in DRG neurons.Cell reports · 2024Article
- Hemodynamic and neurobiological factors for the development of chronic pelvic pain in patients with pelvic venous disorder.Journal of vascular surgery. Venous and lymphatic disorders · 2023Article
- Piezo2 regulates colonic mechanical sensitivity in a sex specific manner in mice.Nature communications · 2023Article
- Upregulation of P2X3 receptors in primary afferent pathways involves in colon-to-bladder cross-sensitization in rats.Frontiers in physiology · 2022Article
- Spinal neuron-glia-immune interaction in cross-organ sensitization.American journal of physiology. Gastrointestinal and liver physiology · 2020Review
- Partners in Crime: NGF and BDNF in Visceral Dysfunction.Current neuropharmacology · 2019Review
- Mechanisms Underlying Overactive Bladder and Interstitial Cystitis/Painful Bladder Syndrome.Frontiers in neuroscience · 2018Review
- Extrinsic Calcitonin Gene-Related Peptide Inhibits Hyperoxia-Induced Alveolar Epithelial Type II Cells Apoptosis, Oxidative Stress, and Reactive Oxygen Species (ROS) Production by Enhancing Notch 1 and Homocysteine-Induced Endoplasmic Reticulum Protein (HERP) Expression.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Regulation of transient receptor potential cation channel subfamily V1 protein synthesis by the phosphoinositide 3-kinase/Akt pathway in colonic hypersensitivity.Experimental neurology · 2017Article
- Elevated expression of transient receptor potential vanilloid type 1 in dorsal root ganglia of rats with endometriosis.Molecular medicine reports · 2017Article
- Colitis-induced bladder afferent neuronal activation is regulated by BDNF through PLCγ pathway.Experimental neurology · 2016Article
- Inflammation and activity augment brain-derived neurotrophic factor peripheral release.Neuroscience · 2016Article
- EXPRESS: Phospholipase C gamma mediates endogenous brain-derived neurotrophic factor - regulated calcitonin gene-related peptide expression in colitis - induced visceral pain.Molecular pain · 2016Article
- Identification of bladder and colon afferents in the nodose ganglia of male rats.The Journal of comparative neurology · 2014Article
- Presynaptic GABAergic inhibition regulated by BDNF contributes to neuropathic pain induction.Nature communications · 2014Article
- Neurotrophin signaling and visceral hypersensitivity.Frontiers in biology · 2014Article
- Article
- Neurobiological mechanisms of pelvic pain.BioMed research international · 2014Review
- Endogenous PI3K/Akt and NMDAR act independently in the regulation of CREB activity in lumbosacral spinal cord in cystitis.Experimental neurology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Colonic inflammation has profound effects on the urinary bladder physiology and produces hypersensitivity of bladder afferent neurons and neurogenic bladder overactivity. Calcitonin gene-related peptide (CGRP) expressed in dorsal root ganglia (DRG) plays an important role in mediating sensory perception following visceral inflammation. In the present study, we determined that the expression of CGRP was increased in bladder afferent neurons in lumbosacral DRG following tri-nitrobenzene sulfonic acid (TNBS)-induced colitis in rat. After colitis, the percentage of bladder afferent neurons expressing CGRP was increased in L1 (61.2+/-2.9% in colitis vs. 37.7+/-5.1% in controls; p<0.05) and S1 DRG (26.3+/-2.3% in colitis vs. 15.5+/-1.9% in controls; p<0.01). We also demonstrated that the expression of tyrosine kinase receptor TrkB was increased in L1 (39.7+/-2.9% in colitis vs. 25.2+/-4.3% in controls; p<0.05) and S1 DRG (45.6+/-3.8% in colitis vs. 38.3+/-3.6% in controls; p<0.01) following colitis. CGRP and TrkB were co-stored in a subpopulation of DRG neurons in control and colitic animals and the number of DRG cells co-expressing CGRP and TrkB was significantly increased in L1 (2.7-fold, p<0.01) and S1 DRG (2.4-fold, p<0.01) following colitis. In cultured DRG, exogenous BDNF application significantly increased CGRP expression, which was blocked by TrkB selective inhibitor K252a. These results suggest that up-regulation of CGRP and TrkB in bladder afferent neurons may play a role in colon-to-bladder cross-sensitization following colitis.
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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.