Effects of ketamine on low intensity tactile sensory input are not dependent upon a spinal site of action.

The development of a technique for studying spinal dorsal horn electrophysiology in intact, awake, drug-free cats enables the study of spinal sites and mechanisms of action of anesthetic and analgesic agents in a system that more closely reflects normal physiology. Using this technique, we reevaluated the effect of ketamine on spinal dorsal horn sensory transmission. The results of our study confirm previous work done in acute preparations. Ketamine (maximum dose 20 mg/kg) did not significantly reduce the response of low threshold (n = 11) dorsal horn neurons to low intensity sensory stimulation. However, that same dose of ketamine did suppress noxiously evoked activity of the two wide dynamic range neurons encountered in the study, while having a varied effect on neurons responsive to proprioceptive input (n = 7). These findings confirm that, in the intact animal with all modulatory systems intact, ketamine "dissociation" of low intensity tactile stimuli does not appear to involve a spinal mechanism of action. The results also support the importance of spinal sites of action for the analgesia produced by ketamine, as well as the importance of distinguishing between the anesthetic and analgesic effects of that drug.