Ben-Eliyahu S, Yirmiya R, Shavit Y, Liebeskind J C
Department of Psychology, University of California, Los Angeles 90024-1563.
Behav Neurosci. 1990 Feb;104(1):235-8. doi: 10.1037//0735-7044.104.1.235.
The suppression of natural killer (NK) cell cytotoxicity by footshock stress can be attenuated by opioid antagonists, implicating endogenous opioids in its mediation. A stress paradigm that induces NK suppression that is not blocked by the opioid antagonist naltrexone is reported. This stress paradigm is also shown to cause analgesia and elevated plasma corticosterone levels that are not attenuated by naltrexone. In the first experiment, a significant suppression of NK cell cytotoxicity after forced swimming was demonstrated in Fischer 344 rats treated with either saline or naltrexone, compared with nonstressed controls. Significantly higher corticosterone levels were evident in both stressed groups. In the second experiment, the same stress paradigm was shown to cause significant analgesia in the tail-flick test, whereas no differences were seen between groups pretreated with saline and naltrexone. It is concluded that opioids need not always be involved in the suppression of NK cell cytotoxicity by stress.
足底电击应激对自然杀伤(NK)细胞细胞毒性的抑制作用可被阿片类拮抗剂减弱,这表明内源性阿片类物质参与了其介导过程。据报道,有一种应激模式可诱导NK细胞抑制,而这种抑制作用不会被阿片类拮抗剂纳曲酮阻断。这种应激模式还会导致镇痛以及血浆皮质酮水平升高,且这些作用不会被纳曲酮减弱。在第一个实验中,与未受应激的对照组相比,用生理盐水或纳曲酮处理的Fischer 344大鼠在强迫游泳后,NK细胞细胞毒性受到了显著抑制。两个应激组的皮质酮水平均显著升高。在第二个实验中,同样的应激模式在甩尾试验中导致了显著的镇痛作用,而用生理盐水和纳曲酮预处理的组之间没有差异。得出的结论是,应激对NK细胞细胞毒性的抑制作用不一定总是涉及阿片类物质。