Harris J A, Westbrook R F, Duffield T Q, Bentivoglio M
School of Psychology, University of New South Wales, Sydney, Australia.
Behav Neurosci. 1995 Apr;109(2):320-8. doi: 10.1037//0735-7044.109.2.320.
Two experiments used c-fos expression as a marker of spinal nociceptive processing to study the neural correlates of hypoalgesic responses to conditioned stimuli (CSs) paired with an aversive event. Immunoreactive (ir) neuronal labeling of Fos, the nuclear protein encoded by the c-fos gene, was examined in the spinal cords of rats killed 2 hr after injection of dilute formalin into a hind paw. Compared with control rats either not conditioned or conditioned in one environment but tested elsewhere, there were significantly fewer Fos-ir neurons in the spinal cords of rats displaying hypoalgesic responses when tested in the presence of aversive CSs. Naloxone abolished hypoalgesic responses and reinstated spinal Fos expression, indicating that aversive CSs activated opioid-based antinociceptive mechanisms. The results confirm that aversive CSs produce hypoalgesia by inhibiting the transmission of ascending nociceptive information.
两项实验使用c-fos表达作为脊髓伤害性处理的标志物，以研究与厌恶事件配对的条件刺激（CSs）引起的痛觉减退反应的神经相关性。在向后爪注射稀释福尔马林2小时后处死的大鼠脊髓中，检查了由c-fos基因编码的核蛋白Fos的免疫反应性（ir）神经元标记。与未进行条件反射或在一个环境中进行条件反射但在其他地方进行测试的对照大鼠相比，在厌恶CSs存在下进行测试时表现出痛觉减退反应的大鼠脊髓中，Fos免疫反应性神经元明显减少。纳洛酮消除了痛觉减退反应并恢复了脊髓Fos表达，表明厌恶CSs激活了基于阿片类药物的抗伤害感受机制。结果证实，厌恶CSs通过抑制上行伤害性信息的传递产生痛觉减退。
