Gogas K R, Cho H J, Botchkina G I, Levine J D, Basbaum A I
Department of Anatomy, University of California at San Francisco, CA 94143 USA Department of physiology, University of California at San Francisco, CA 94143 USA Department of Medicine, University of California at San Francisco, CA 94143 USA Oral Surgery, University of California at San Francisco, CA 94143 USA W.M. Keck Foundation Center for Integrative Neuroscience, University of California at San Francisco, CA 94143 USA.
Pain. 1996 Apr;65(1):9-15. doi: 10.1016/0304-3959(95)00141-7.
In previous studies, we reported that supraspinally administered DAMGO, a mu-opioid agonist, produces a dose-related, naloxone-reversible inhibition of formalin-evoked pain behaviors and spinal cord Fos-like immunoreactivity (FLI) in the rat spinal cord. Although these results support the hypothesis that activation of supraspinal mu-opioid receptors produces antinociception by increasing the activity of bulbospinal inhibitory pathways, other studies suggest that supraspinal morphine decreases rather than increases descending inhibitory control. In the present study, we specifically examined the effect of intracerebroventricular (i.c.v.) injection of morphine in the rat. Supraspinal morphine produced a dose-related, naloxone-reversible inhibition of both formalin-evoked behaviors nd spinal cord FLI. Although the magnitude of the antinociception produced by i.c.v. morphine in the formalin test was significantly correlated with the numbers of FLI neurons in the spinal cord, the lowest dose of i.c.v. morphine tested (0.70 nmol) produced a significant reduction of FLI in the superficial laminae without producing behavioral antinociception, which is consistent with our hypothesis that noxious stimulus-evoked Fos expression in the superficial laminae is a poor predictor of the magnitude of pain behavior. These data support the hypothesis that the antinociceptive effects of supraspinally administered morphine result from an increase in descending inhibitory control.
在先前的研究中，我们报道，经脊髓以上给予μ阿片受体激动剂DAMGO，可产生剂量相关的、纳洛酮可逆转的对福尔马林诱发的疼痛行为以及大鼠脊髓中Fos样免疫反应性（FLI）的抑制作用。尽管这些结果支持如下假说：脊髓以上μ阿片受体的激活通过增强延髓脊髓抑制性通路的活性而产生抗伤害感受作用，但其他研究提示，脊髓以上给予吗啡会降低而非增强下行抑制性控制。在本研究中，我们专门检测了脑室内（i.c.v.）注射吗啡对大鼠的影响。脊髓以上给予吗啡可产生剂量相关的、纳洛酮可逆转的对福尔马林诱发的行为和脊髓FLI的抑制作用。尽管在福尔马林试验中i.c.v.注射吗啡所产生的抗伤害感受程度与脊髓中FLI神经元的数量显著相关，但所检测的最低剂量i.c.v.吗啡（0.70 nmol）可使浅层的FLI显著减少，却未产生行为性抗伤害感受，这与我们的假说相符，即有害刺激诱发的浅层Fos表达并不能很好地预测疼痛行为的程度。这些数据支持如下假说：脊髓以上给予吗啡的抗伤害感受作用源于下行抑制性控制的增强。
