Abstract
The role of the ventral noradrenergic bundle (VB) was examined in relation to endorphins in the control of nociception in the rat. Selective, bilateral destruction of the VB produced a substantial fall in hypothalamic levels of noradrenaline [norepinephrine]. On day 4 postsurgery, VB-lesioned rats displayed a pronounced elevation in basal nociceptive threshold. This was reversible by the specific opioid antagonist, naloxone, indicating its mediation by endorphins. It was unaffected by dexamethasone, a suppressor of corticotrophic secretion of .beta.-endorphin, indicating that this pituitary pool of .beta.-endorphin was not responsible. On day 12, the elevation in nociceptive threshold had disappeared and neither the time course nor the intensity of the antinociception elicited by acute stress or various doses of morphine was attenuated in VB-lesioned as compared to sham rats. The VB may influence nociceptive thresholds via an interaction with a CNS endorphinergic network. The VB does not mediate a significant component of the antinociception generated by either morphine or stress.