Pregabalin decreases visceral pain and prevents spinal neuronal activation in rats
- CURE/Digestive Diseases Research Center and Center for Neurovisceral Sciences and Women’s Health, Department of Medicine, Division of Digestive Diseases, University of California Los Angeles, and VA Greater Los Angeles Healthcare System, Los Angeles, California, USA
- Correspondence to:
Dr Mulugeta Million
CURE/CNS Building 115, Room 118B, VA Greater Los Angeles Healthcare System, 1130 Wilshire Blvd, Los Angeles, CA 90073, USA;
We read the recent article by Houghton et al (Gut 2007, Apr 19 [Epub ahead of print]), reporting that pregabalin, a new generation of α2δ ligand, increased sensory thresholds to normal levels in 26 patients with irritable bowel syndrome (IBS) and baseline rectal hypersensitivity, in a randomised double blind, placebo controlled, parallel group study. The authors concluded that α2δ ligands are worthy of further physiological and clinical investigations for diseases affecting gut sensory function. Experimental studies to date indicate that pregabalin prevents colorectal allodynia and hyperalgesia in rats exposed to intracolonic trinitrobenzene-sulphonic acid1 or septic shock.2 Visceral hyperalgesia and symptoms in IBS are, however, characterised by the absence of overt colonic damage or mucosal abnormality. In the study we describe here, pregabalin given orally in a rat non-inflammatory model of repeated tonic colorectal-distension-induced hypersensitivity3 prevented visceral hyperalgesia and blunted lumbosacral spinal neurone activation.
Adult male Sprague–Dawley rats with or without electrodes implanted in the abdominal muscles were given orally (po) either vehicle (water, 1 ml/rat) or pregabalin (10 or 30 mg/kg; Parke Davis, Fresnes, France) and placed individually in Bollman cages. After a 60 minute stabilisation period, basal abdominal contractions were monitored for 10 minutes, then isobaric colorectal distension …