Antinociception produced by mu opioid receptor activation in the amygdala is partly dependent on activation of mu opioid and neurotensin receptors inthe ventral periaqueductal gray

Exposure to stressful or fear-inducing environmental stimuli activates desc ending antinociceptive systems resulting in a decreased pain response to pe ripheral noxious stimuli. Stimulating mu opioid receptors in the basolatera l nucleus of the amygdala (BLA) in anesthetized rats produces antinocicepti on that is similar to environmentally induced antinociception in awake rats . Recent evidence suggests that both forms of antinociception are mediated via projections from the amygdala to the ventral periaqueductal gray (PAG). In the present study, we examined the types of neurochemicals released in the ventral PAG that may be important in the expression of antinociception produced by amygdala stimulation in anesthetized rats. Microinjection of a mu opioid receptor agonist into the BLA resulted in a time dependent increa se in tail flick latency that was attenuated by preadministration of a mu o pioid receptor or a neurotensin receptor antagonist into the ventral PAG. M icroinjection of a delta, opioid receptor antagonist or an NMDA receptor an tagonist into the ventral PAG was ineffective. These findings suggest that amygdala stimulation produces antinociception that is mediated in part by o pioid and neurotensin release within the Ventral PAG. (C) 2000 Elsevier Sci ence BN. All rights reserved.