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This Article Full Text Full Text (PDF) All Versions of this Article: 586/21/5247    most recent jphysiol.2008.159731v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by De Schepper, H. U. Articles by De Man, J. G. PubMed PubMed Citation Articles by De Schepper, H. U. Articles by De Man, J. G. Related Collections Integrative Related Article

¹ Laboratory of Experimental Medicine and Pediatrics, Division of Gastroenterology, Faculty of Medicine, University of Antwerp, Universiteitsplein 1, Antwerp B-2610, Belgium
² Research Group Cell Biology and Histology, Department of Veterinary Sciences, University of Antwerp, Groenenborgerlaan 171, Antwerp B-2020, Belgium
³ Laboratory of Pharmacology, Department of Pharmacy, University of Antwerp, Universiteitsplein 1, Antwerp B-2610, Belgium

Patients with inflammatory bowel disease often suffer from gastrointestinal motility and sensitivity disorders. The aim of the current study was to investigate the role of transient receptor potential of the vanilloid type 1 (TRPV1) receptors in the pathophysiology of colitis-induced pelvic afferent nerve sensitization. Trinitrobenzene sulphate (TNBS) colitis (7.5 mg, 30% ethanol) was induced in Wistar rats 72 h prior to the experiment. Single-fibre recordings were made from pelvic nerve afferents in the decentralized S1 dorsal root. Fibres responding to colorectal distension (CRD) were identified in controls and rats with TNBS colitis. The effect of the TRPV1 antagonist N-(4-tertiarybutylphenyl)-4-(3-chlorophyridin-2-yl)tetrahydropyrazine-1(2H)carboxamide (BCTC; 0.25–5 mg kg^–1) or its vehicle (hydroxypropyl-β-cyclodextrin) was tested on the afferent response to repetitive distensions (60 mmHg). Immunocytochemical staining of TRPV1 and NF200, a marker for A-fibre neurons, was performed in the dorsal root ganglia L6–S1. TNBS colitis significantly increased the response to colorectal distension of pelvic afferent C-fibres. BCTC did not significantly affect the C-fibre response in controls, but normalized the sensitized response in rats with colitis. TNBS colitis increased the spontaneous activity of C-fibres, an effect which was insensitive to administration of BCTC. TNBS colitis had no effect on A-fibres, nor was their activity modulated by BCTC. TNBS colitis caused an immunocytochemical up-regulation of TRPV1 receptors in the cell bodies of pelvic afferent NF200 negative neurons. TRPV1 signalling mediates the colitis-induced sensitization of pelvic afferent C-fibres to CRD, while A-fibres are neither sensitized by colitis nor affected by TRPV1 inhibition.

(Received 14 July 2008; accepted after revision 27 August 2008; first published online 28 August 2008)
Corresponding author J. G. De Man: Laboratory of Experimental Medicine and Pediatrics, Division of Gastroenterology, Faculty of Medicine, University of Antwerp, Universiteitsplein 1, 2610 Antwerp, Belgium. Email: joris.deman{at}ua.ac.be

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