EFFECTS OF ANTEROLATERAL SPINAL LESIONS ON ESCAPE RESPONSES OF RATS TO HINDPAW STIMULATION

In order to determine the effects of spinal cord lesions on nociceptive sensitivity of rodents, methods were developed to assess the speed of operant escape responses to electrocutaneous stimulation (ES). ES was delivered across the dorsal and ventral surfaces of either hindpaw, producing a current path through deep tissues. In order to guide establishment of a range of stimulus intensities for this manner of stimulation, a preliminary human psychophysical experiment was conducted with stimulation between the dorsal and ventral surfaces of a finger. For the human subjects, detection thresholds averaged 0.13 mA, and thresholds for a sharp (but nonpainful) sensation were 0.42 mA. Levels of stimulation between these thresholds for detection and a sharp quality elicited sensations of tingle or itch. Thresholds for reports of pain averaged 0.67 mA. On the basis of these results, intensities of ES ranging from 0.05 to 1.0 mA were presented to the feet of rats that were trained to perform an escape response with one forelimb. Thresholds for escape averaged slightly less than 0.1 mA; responding was consistent at 0.4 mA; and response probability and speed were maximal at approximately 0.8 mA. Thus, the rats responded aversively at intensities below those rated as sharp or painful by the human subjects, but the speed of escape reached a plateau at intensities that were above pain threshold for the human subjects. Unilateral thoracic lesions of the lateral spinal column of rats produced a contralateral hypalgesia. Escape thresholds were elevated, and the speed of escape responses to all intensities was reduced. This effect depended upon interruption of axons in the middle and anterior portions of one lateral column, corresponding to the location of long ascending pathways for nociception, including the spinothalamic tract. The speed of escape re spending increased over 20 weeks of postoperative resting of animals with the largest lesions. This confirms results obtained previously from monkeys (by means of a similar paradigm), and corresponds to clinical reports of humans who have received spinal lesions for control of intractable pain. Thus, the location and organization of nociceptive pathways in the spinal cord of rodents appear to be similar to those of primates, and similar adaptations occur following interruption of these pathways.