In the anesthetized rat, systemic cocaine at an analgesic dose (25 mg/kg, IP) had no general influence on spontaneous activity in nociceptive spinoreticular tract neurons or in rostrally projecting low-threshold mechanoreceptive neurons of the spinal dorsal horn. Peripherally evoked activity was moderately (mean: 30%) reduced in 43% (6/14) of the spinoreticular tract neurons, whereas in 50% of them there was no marked change in evoked activity by cocaine. Evoked activity was slightly reduced in 25% (2/8) of the low-threshold mechanoreceptive neurons and not changed in 75% of them. The suppressive effect of a distant conditioning noxious stimulus on responses to spinoreticular tract neurons was enhanced by cocaine in 3/6 of the spinoreticular tract neurons. Primary afferent terminal excitability of A-fibers was slightly increased following cocaine as indicated by the increased amplitude (mean: 24%) of the antidromically evoked compound action potential recorded from the sural nerve. It is concluded that the previously shown marked enhancement of spontaneous activity in the bulborecticular formation is generated supraspinally. Thus, while cocaine-induced analgesia appears to be due primarily to supraspinal mechanisms, the present results suggest that spinal mechanisms are also involved possibly presynaptically.
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