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Recent clinical studies have demonstrated that a midline lesion of the dorsal columns (DC, limited midline myelotomy) reduces pain of visceral origin in patients with pelvic cancer. Animal experiments showed that a DC lesion leads to decreased activation of thalamic neurons by visceral stimuli, lowers the impact of noxious colon stimulation in behavioral tests and suggested that the effect is mediated mainly by postsynaptic DC neurons. In the present experiments we examined the effect of bilateral DC or ventrolateral (VL) spinal cord lesions on visceromotor reflex EMG activity evoked by graded colorectal distention (30, 60, 80 mmHg) under control conditions and after colon inflammation with mustard oil. The colon inflammation increased significantly the visceromotor responses so that the response to a 30 mmHg distention was larger than that produced by 80 mmHg before inflammation. The DC lesion did not affect the visceromotor reflex response under control conditions but reduced the increased responses after colon inflammation back to control levels and prevented the potentiation of the reflex responses by colon inflammation when performed before the inflammation. Our results suggest that the role of the DC pathway in transmission of visceral pain is augmented under inflammatory conditions when symptoms of visceral allodynia and hyperalgesia may be present. The VL lesions eliminated the visceromotor reflex, presumably by interrupting a facilitatory pathway that involves the brain stem.