NO参与介导吗啡戒断大鼠脊髓神经元敏感化

运用Fos免疫组织化学、NADPH－d组织化学、F/NADPH－d双标、鞘内注射和反义寡核苷酸技术，观察吗啡戒断大鼠脊髓神经元活动变化及NO在其中的作用，结果发现：非吗啡依赖大鼠急性应用纳洛酮和吗啡依赖大鼠脊髓水平Fos-LI和NADPH－d阳性神经元表达与对照组相比无明显变化，二者也无Fos／NADPH－d双标神经元表达；吗啡依赖纳洛酮催促戒断大鼠脊髓Fos-LI、NADPH－d阳性神经元、纤维和终末表达明显增加，且出现Fos／NADPH－d双标神经元表达。Fos-LI和Fos／NADPH－d双标神经元呈现双侧脊髓全层分布，NADPH－d阳性神经元、纤维和终末主要位于双侧脊髓背角浅层。鞘内注射NOS抑制剂L－NA和nNOS反义寡核苷酸均明显降低吗啡依赖大鼠纳洛酮催促戒断症状评分，减少吗啡戒断大鼠脊髓Fos-LI表达。上述结果提示：NO参与介导吗啡戒断大鼠脊髓神经元敏感化。

NO involvement in mediation of spinal neuron sensitization in morphine-withdrawal rats

The effects of nitric oxide (NO) on the activation of spinal cord neurons were studied using immunocytochemistry, intrathecal injection and antisense oligonucleotides (AS ONs) techniques in morphine withdrawal rats. Acute administration of naloxone and chronic administration of morphine changed neither the expression of Fos LI and NADPH d positive neurons nor the expression of Fos/NADPH d double labeled neurons in the spinal cord of rats. Fos LI, NADPH d positive and Fos/NADPH d double labeled neurons were increased significantly in number in morphine withdrawal rats and they were observed in all the laminae of the spinal cord. Intrathecal injection of L NA, nNOS antisense oligonucleotides significantly inhibited the expression of Fos LI in the spinal cord and decreased the scores for morphine withdrawal symptoms in morphine withdrawal rats, but not in nNOS S group. The results suggest that NO mediates the spinal neuron sensitization in morphine withdrawal rats.