Naloxone-reversible analgesia produced by microstimulation of the arcuate nucleus of the hypothalamus in pentobarbital-anesthetized rats.

Suppression of the tail flick response to noxious heat and paw withdrawal response to noxious pressure were produced by electrical stimulation of arcuate nucleus of the hypothalamus (ARH) in pentobarbital anesthetized rats. Systemic administration of naloxone (2 mg/kg) greatly antagonized the ARH stimulation-produced inhibition of both algesic reflexes. The thresholds of stimulation for inhibition of two spinal nociceptive reflexes in the lightly anesthetized state were not significantly different from the thresholds of stimulation at the same ARH sites in the awake state in the same animals. These findings provide evidence establishing the (1) usefulness of the anesthetized rat model for investigation of antinociceptive mechanisms; (2) the involvement of endogenous opioid mechanisms in mediating ARH stimulation-produced analgesia.