Millan M J, Millan M H, Herz A
Department of Neuropharmacology, Max-Planck-Institut für Psychiatrie, Kraepelinstrasse 2, D-8000 Munich 40 F.R.G.
Pain. 1982 Sep;14(1):21-32. doi: 10.1016/0304-3959(82)90077-X.
The present paper examines the role of the ventral noradrenergic bundle (VB) 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. On day 4 post-surgery, VB-lesioned rats displayed a pronounced elevation in basal nociceptive threshold. This proved to be reversible by the specific opioid antagonist, naloxone, evidential of its mediation by endorphins. It was, however, unaffected by dexamethasone, a suppressor of corticotrophic secretion of beta-endorphin, indicative that this pituitary pool of beta-endorphin was not responsible. On day 12, at which time the elevation in nociceptive threshold had disappeared, 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. These data are evidential that the VB may influence nociceptive thresholds via an interaction with a CNS endorphinergic network. They demonstrate, further, that the VB does not mediate a significant component of the antinociception generated by either morphine or stress.
本文研究了腹侧去甲肾上腺素能束（VB）在大鼠痛觉控制中与内啡肽相关的作用。选择性双侧损毁VB导致下丘脑去甲肾上腺素水平大幅下降。术后第4天，VB损伤大鼠的基础痛觉阈值显著升高。这被证明可被特异性阿片拮抗剂纳洛酮逆转，表明其由内啡肽介导。然而，它不受地塞米松的影响，地塞米松是β-内啡肽促肾上腺皮质激素分泌的抑制剂，这表明垂体中的β-内啡肽库与此无关。在第12天，此时痛觉阈值的升高已消失，与假手术大鼠相比，VB损伤大鼠由急性应激或各种剂量吗啡引起的抗伤害感受的时间进程和强度均未减弱。这些数据证明VB可能通过与中枢神经系统内啡肽能网络相互作用来影响痛觉阈值。它们进一步证明，VB并不介导吗啡或应激产生的抗伤害感受的重要组成部分。
