Analysis of lumbar dorsal spinal potentials evoked by electrical stimulation of the colon and their changes induced by high-frequency stimulation or ischemia in rats

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The clinical-related input and processing of intestinal afferents to the spinal cord is not well known. This study aims to develop an electrophysiological experimental animal model to study spinal cord afferents from the colon during clinical-related conditions such as hyperexcitability or ischemia. Spinal cord evoked potentials (SCEP) were elicited by colonic stimulation in ten male adult Sprague-Dawley rats anesthetized with thiobarbital, 60 mg kg-1 i.p. After laminectomy (T11 to L5), a tungsten electrode (500 μm; <50Ω) was placed in the spinal dorsum to record SCEP induced by bipolar electrical stimulation of colon mucosa (basal 30 V; 1 ms) at low (0.2 Hz; 10 min) or high (5 Hz; 5 min) frequency. In 3 experiments, after the basal recording, a respiratory arrest was induced by D-tubocurarine to evaluate the ischemia effects. The SCEPs were stable and reliable (n=310), displaying a N1 wave (delay: 3.9±0.1 ms; amplitude 7.78±0.39 μV) and P1 wave (delay 9.96±0.14 ms; amplitude 2.97±0.21 μV). Colonic high-frequency stimulation induced an amplitude increase in both +11% (N1) and +23.7% (P1) (p<0.001). The ischemia induced a linear decay of both wave amplitudes more intense for the P1 wave. sensitive. These results denote the intense colonic input to the lumbar dorsal spinal cord, the presence of spinal sensory potentiation mechanisms induced by colonic high frequency stimulation, and the high oxygen dependency of the neuronal networks involved in the N1 and P1 wave generation. This experimental model could contribute to the study of visceral pain and inflammation, allowing the electrophysiological evaluation of experimental treatment response in experimental colon disease models.

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