Abstract
Central sensitization is one of the mechanisms proposed to explain the development and spread of secondary hypersensitivity following tissue injury. It accompanies skin, joint as well as visceral organ inflammation, but as yet was not evidenced in functional abdominal disorders. Aim: In this study, we use electrophysiological means to test the hypothesis that colorectal hypersensitivity in a new animal model of chronic functional visceral pain is associated with central neuronal sensitization. Methods: Experiments were done on 20 adult male Sprague Dawley rats (300-350 gms). Thirteen rats received colon irritation as neonates (Colorectal distension: CRD, n=6; Mustard Oil: MO, n=7) and developed chronic visceral hypersensitivity to CRD and 7 rats served as controls. Under anesthesia (Pentobarbital 50 mglkg, ip followed by 5mg/kglhr, iv), a laminectomy was made to expose the spinal cord at the level of the L6-SI segments. Extracellular single neuron recordings were made using a high impedance tungsten microelectrode. Isolated neurons were tested with a range of CRD (20, 40, 60 and 80 mmHg) induced by inflating a balloon inserted rectally into the descending colon. The responses of the colonsensitive neurons to CRD and to somatic stimulation were recorded and compared between groups. Results: A total of 67 neurons (Control, n=25; CRD, n= 19; MO, n=22) were isolated in the gray matter of the spinal cord at the level of L6-SI and were tested with graded CRD and somatic stimulation. The distribution of the somatic receptive fields was similar in all groups. Neurons isolated in rats with neonatal colon irritation (both groups) showed on average a significantly higher baseline activity (24.7+/2.8) compared to neurons in control rats(6.8 +/1.3) in addition to significantly higher responses to CRD and somatic stimulation (p<0.05). Conclusions: Our results indicate that in rats, chronic visceral hypersensitivity residual to neonatal colon irritation is associated with central neuronal sensitization manifested by a heightened baseline firing rate and increased responses to CRD and somatic stimulation. Reducing this neuronal sensitization may be a promising start to target chronic visceral pain.
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