Lumbar intrathecal administration of naloxone antagonizes analgesia produced by electrical stimulation of the hypothalamic arcuate nucleus in pentobarbital-anesthetized rats.

In lightly pentobarbital-anesthetized and acutely-prepared rats, electrical stimulation within the arcuate nucleus of the hypothalamus consistently inhibited the tail-flick responses to noxious heating of the tail. The opioid receptor antagonist, naloxone hydrochloride applied intrathecally at the lumbar level, at dose of 20 micrograms, reversed this inhibition without affecting the baseline pain threshold. The same dose of naloxone, applied to the cervical subarachnoid space, had no effect on the inhibitory modulation by the arcuate nucleus. Naloxone, at doses 2- to 4-fold greater than the intrathecal dose, did not modify the suppression of the tail-flick, when given systemically. With the doses ranging from 5 to 40 micrograms, naloxone showed a dose-dependent blockade of the inhibition produced by stimulation of the arcuate nucleus. These results indicate that an endogenous opioid system is most likely involved in the descending inhibition of spinal nociceptive reflexes, resulting from stimulation of the arcuate nucleus of the hypothalamus.