1. Noxious stimuli have been shown to produce a diffuse inhibition of nociresponsive neurons in the spinal and trigeminal dorsal horns. The present study sought to extend these electrophysiological studies of diffuse noxious inhibitory controls (DNIC) by determining the effect of a spatially remote noxious stimulus on behavioral measures of nociception. Changes in latency for hindpaw withdrawal and tail flick reflexes were measured in lightly halothane-anesthetized or awake, spinally transected rats before, during, and after application of a spatially remote noxious stimulus. 2. Surprisingly, in no case did application of a spatially remote noxious stimulus inhibit the hindpaw withdrawal reflex. The latency for this reflex was either reduced or did not change when the tail or contralateral hindpaw was placed in hot water (50°C) or when a noxious pinch was applied to the ear. In contrast, the latency for the tail flick reflex was consistently increased when the hindpaw was placed in hot water. Both the hindpaw reflex facilitation and the tail flick reflex inhibition produced by a noxious conditioning stimulus were attenuated in spinally transected rats indicating supraspinal modulation of both reflexes. 3. In addition, and consistent with the work of others, placing the tail in hot water reduced the evoked activity of convergent neurons in both the trigeminal and lumbar spinal dorsal horns. Thus inhibition of the activity of nociresponsive neurons in the dorsal horn is consistent with inhibition of the tail flick reflex, but not with facilitation of the hindpaw withdrawal reflex. 4. The reduction in hindpaw withdrawal latency concomitant with inhibition of nociresponsive neurons in the dorsal horn of the spinal cord indicates parallel inhibitory and facilitatory modulation of the hindpaw reflex. Because there is no evidence that facilitation of the hindpaw withdrawal reflex occurs via influences on dorsal horn neurons (nociresponsive neurons in the dorsal horn are almost universally inhibited; see DISCUSSION), presumably, a noxious conditioning stimulus primes interneurons interposed between dorsal horn nociresponsive neurons and motoneurons, thereby allowing these neurons to respond to the muted nociceptive message from the dorsal horn. Simultaneous modulation of the hindpaw withdrawal reflex in the dorsal and ventral horns produced by a spatially remote noxious stimulus could allow pain sensation to be inhibited while leaving escape reactions intact.
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