Millan M J, Przewłocki R, Millan M H, Herz A
Pharmacol Biochem Behav. 1983 Jun;18(6):901-7. doi: 10.1016/s0091-3057(83)80013-6.
Bilateral, radio-frequency destruction of the ventro-medial posterior hypothalamus (VMPH) resulted, as compared to sham-operated and control rats and evaluated in the tail-flick and vocalization tests, in a significant decrease in basal nociceptive threshold on day 4 post-surgery. By day 12, however, no significant difference between sham and lesioned rats was seen. At this time the antinociception elicited by either acute foot-shock or cold-water-immersion stress was profoundly attenuated. The antinociceptive response to various doses of morphine was not, in contrast, diminished. As established by use of radioimmunoassay, these lesions did not significantly alter hypothalamic levels of beta-endorphin, met-enkephalin, dynorphin or alpha-neo-endorphin. They did, however, produce a pronounced and significant fall in the hypothalamic content of substance P. These data are indicative that the VMPH may, via a mechanism not involving endorphins, be of importance in the determination of basal nociceptive threshold and in the generation of stress-, but not morphine-, evoked antinociception. The relationship of these findings to the interconnections of the VMPH, and to the possible significance of substance P and the pituitary in nociceptive processes, is discussed.
与假手术组和对照组大鼠相比，双侧腹内侧后下丘脑（VMPH）经射频毁损后，在甩尾试验和发声试验中评估发现，术后第4天基础伤害性感受阈值显著降低。然而，到第12天，假手术组和毁损组大鼠之间未观察到显著差异。此时，急性足部电击或冷水浸泡应激所引发的抗伤害感受作用显著减弱。相比之下，对不同剂量吗啡的抗伤害感受反应并未减弱。通过放射免疫测定确定，这些毁损并未显著改变下丘脑β-内啡肽、甲硫氨酸脑啡肽、强啡肽或α-新内啡肽的水平。然而，它们确实使下丘脑P物质含量显著下降。这些数据表明，VMPH可能通过一种不涉及内啡肽的机制，在基础伤害性感受阈值的确定以及应激诱发而非吗啡诱发的抗伤害感受的产生中发挥重要作用。本文讨论了这些发现与VMPH的相互联系，以及P物质和垂体在伤害性感受过程中的可能意义之间的关系。
