Continuous naloxone administration via osmotic minipump decreases autotomy but has no effect on nociceptive threshold in the rat.

Rats with unilaterally sectioned sciatic nerves were continuously administered naloxone HCl (80 or 800 micrograms/h) or equivalent volumes of saline (1 or 10 microliters/h) subcutaneously via osmotic minipumps over a 2 or 5 week period. Rats receiving 80 micrograms/h naloxone for 5 weeks exhibited significantly less self-mutilation (autotomy) of the denervated foot than saline controls or rats receiving 80 micrograms/h naloxone for 2 weeks. The nociceptive threshold of intact rats infused with the same dose of naloxone was tested on a hot plate. In these animals there was no influence on the nociceptive threshold during naloxone administration for 1 week. Autotomy was also reduced in rats infused with 800 micrograms/h naloxone. The nociceptive threshold of intact rats infused with this dose of naloxone or an equivalent volume of saline (10 microliters/h) was increased, suggesting that the presence of the larger osmotic pump caused analgesia.

Stress-related pain behavior in rats with peripheral nerve injuries.

The effects of cold stress were studied on rats with unilaterally sectioned sciatic nerves. Behaviors suggestive of pain occurred in a number of these animals. These behaviors vanished when removing the rats from the stressful environment. Some severely painful syndromes in man might in part be due to mechanisms similar to those underlying the described behaviors in rats.

The effect of dorsal column stimulation on the nociceptive response of dorsal horn cells and its relevance for pain suppression.

The effect of single and repetitive electrical stimulation of the dorsal columns on cells in laminae IV and V of the ipsilateral dorsal horn at S1 was examined in spinalized cats. About two-thirds of the cells responded to thermal nociceptive cutaneous stimulation and of these most responded also to low threshold mechanical stimulation. The other one-third of the cells were innervated by mechanoreceptors including type I or Haarscheiben. A single shock to the dorsal columns typically caused short latency activation of the cells, followed by inhibition lasting about 100 msec. Several minutes of repetitive dorsal column stimulation (DCS) at 3 Hz or 50 Hz had no prolonged effect on about two-thirds of the cells. The rest of the cells were less responsive for up to 30 min after the cessation of 50 Hz. Assuming that the studied interneurons have a pain-mediating function, the results indicate that some cumulative and poststimulatory DCS suppression of pain may be ascribed to spinal mechanisms. The more effective and longer lasting suppression produced by DCS in pain patients would, however, be dependent on other types of interneurons, on suprasegmental loops and/or on effects on pathophysiological mechanisms which may be operative in the chronic pain state. The lack of cumulative inhibition in most of the cells in this study is compatible with the previous observation of a retained perception of acute pain during DCS in man.