SPINAL MECHANISMS UNDERLYING PERSISTENT PAIN AND REFERRED HYPERALGESIA IN RATS WITH AN EXPERIMENTAL URETERAL STONE

Spinal neurons processing information from the ureter have been charac terized in rats 1-4 days after the implantation of an experimental ure teric stone and compared with those of normal rats. The effects of a c onditioning noxious stimulation of the ureter in the presence of the h yperalgesia evoked by the calculosis also were examined. Extracellular recordings were performed at the T-12-L-1 segments of the spinal cord . In rats with calculosis, more neurons expressed a ureter input (53 v s. 42% in normal rats); such cells being more likely to show backgroun d activity, at a higher rate than normals (6.6 +/- 1.2 vs. 3.2 +/- 0.9 spikes/s; mean +/- SE) and increasing with the continuing presence of the stone. The threshold pressure for a ureteric response was higher than in normal rats (79 +/- 5 vs. 54 +/- 4 mmHg) but the neurons faile d to encode increasing intensities of stimulation. Thirty-five percent of the neurons with exclusively innocuous somatic receptive fields ha d a ureter input in rats with calculosis, whereas none were seen in no rmal rats. A noxious ureteric distention applied to neurons with meter input evoked a complex mixture of increases and decreases in somatic receptive held size and/or somatic input properties markedly different from the generalized increases in excitability seen when such a stimu lus was applied to normal animals. We conclude that the presence of a ureteric stone evokes excitability changes of spinal neurons (enhanced background activity, greater number of ureter-driven cells, decreased threshold of convergent somatic receptive fields), which likely accou nt for the referred hyperalgesia seen in rats with calculosis. However , further noxious visceral input occurring in the presence of persiste nt hyperalgesia produces selective changes that cannot be explained by a generalized excitability increase and suggest that the mechanisms u nderlying maintenance of hyperalgesia include alteration of both centr al inhibitory and excitatory systems.