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在痛觉调制中 ,脑干下行抑制系统被认为至少包括去甲肾上腺素 (NE)能和 5 羟色胺 (5 HT)能两类下行投射纤维 ,在脊髓背角中实现对痛信号上传的阻断作用。对于NE能或 5 HT能末梢是否要通过内啡肽能中间神经元介导其镇痛作用 ,现在仍然存在争议。福尔马林皮下注射是一种常用于行为学观察的化学性慢痛模型 ,本实验则采用乌拉坦麻醉的Wistar大鼠 ,用常规细胞外放电记录技术 ,以后肢脚掌皮下注射福尔马林 (5 % ,5 0 μl)诱发的丘脑束旁核 (PF)神经元伤害性放电的改变作为背角中痛信号传递过程受调制的指标 ,观察鞘内注入NE和 5 HT对于福尔马林诱发的PF神经元伤害性放电的影响以及阿片受体拮抗剂纳络酮 (NAL)对于NE和 5 HT效应的影响。结果发现 :①皮下注射福尔马林可诱发PF神经元产生同行为反应类似的双相伤害性放电 ;②鞘内注入NE(6nmol,10 μl)或 5 HT(12 0nmol,10 μl)可显著抑制上述伤害性放电的第二相 ;③鞘内注入NAL(5 0nmol,10 μl)对伤害性放电第二相无明显影响 ;④鞘内注入同量的NAL能取消NE(6nmol,10 μl)引起的对伤害性放电的抑制效应而不能取消 5 HT(12 0nmol,10 μl)引起的对伤害性放电的抑制效应。上述结果表明 ,鞘内给予的NE可能要通过内啡肽能中间神经元释放阿片样物质以实现镇痛作用
In pain modulation, the descending inhibitory system of the brainstem is thought to include at least two types of down-projected fibers, norepinephrine (NE) and serotonin (5HT), which block the uploading of pain signals in the spinal dorsal horn . It is still controversial whether NE or 5 HT endings can mediate their analgesic effects via endorphin-interneurons. Formalin subcutaneous injection is a commonly used chemical behavioral observation of chronic pain model, the experiment is the use of urethane anesthesia in Wistar rats, using conventional extracellular discharge recording technique, the hind paw subcutaneous injection of formalin (5%, 50 μl) induced neurotrophic changes in thalamic parafascicular nucleus (PF) neurons as an indicator of modulation of pain signal transmission in the dorsal horn. The effects of intrathecal injection of NE and 5 HT on formalin Induced neuronal firing in PF and the effect of opioid receptor antagonist naloxone (NEAL) on the NE and 5 HT effects. The results showed that: (1) Subcutaneous injection of formalin could induce PF neurons to generate biphasic nociceptive discharge with similar behavior; (2) intrathecal injection of NE (6 nmol, 10 μl) or 5 HT (120 nmol, 10 μl) (5 nmol, 10 μl) had no significant effect on the second phase of noxious discharge. (4) Injecting the same amount of NAL intrathecally could abolish NE (6 nmol, 10 μl) Induced inhibitory effect on nociceptive discharge but not the inhibitory effect on nociceptive discharge caused by 5 HT (120 nmol, 10 μl). The above results indicate that intrathecal administration of NE may be required to release opioids through endorphin-interneurons for analgesic effect