Hu W H, Lee F C, Wan X S, Chen Y T, Jen M F
Institute of Basic Medical Sciences, Peking Union Medical College, Beijing, People's Republic of China.
Neurosci Lett. 1996 Jan 12;203(1):13-6. doi: 10.1016/0304-3940(95)12246-x.
Nitric oxide (NO) mediation in the spinal cord injury induced by intrathecal (i.t.) dynorphin (Dyn) administration was studied with NADPH-diaphorase (Nd) histochemistry. Normally, there was rarely NO synthase (NOS) activity in spinal cord motomeurons, and Dyn A(1-17) 10 nmol, which produced only transient paralysis, did not induce Nd/NOS expression in ventral horn cells. After a paralyzing dose of i.t. Dyn A(1-17) 20 nmol, which definitely produced permanent paraplegia and neuronal death, Nd/NOS began to express in motoneurons at 30 min, increased in numbers and intensities at 2-4 h and persisted up to 8 h. Most of Nd/NOS motoneurons disappeared at 24 h coincident with the neuronal death. Quite a few intensively-stained Nd-positive small cells and swollen varicosities became visible only in rats with permanent paraplegia and neuronal death, beginning at 2 h, maximizing at 3-4 h and remaining up to 24 h. These results suggest that NOS expression was induced in the ventral horn of spinal cord, including small cells and varicosities as well as motoneurons closely correlated in time and degree with pathological changes in motoneurons caused by spinal Dyn neurotoxicity.
采用还原型辅酶Ⅱ黄递酶（Nd）组织化学方法，研究鞘内注射强啡肽（Dyn）诱导脊髓损伤过程中一氧化氮（NO）的介导作用。正常情况下，脊髓运动神经元中很少有一氧化氮合酶（NOS）活性，10 nmol的强啡肽A（1-17）仅产生短暂性麻痹，并未诱导腹角细胞中Nd/NOS表达。鞘内注射20 nmol能导致永久性截瘫和神经元死亡的致瘫剂量强啡肽A（1-17）后，Nd/NOS在30分钟时开始在运动神经元中表达，2-4小时数量和强度增加，并持续至8小时。大多数Nd/NOS运动神经元在24小时时消失，与神经元死亡同时发生。只有在发生永久性截瘫和神经元死亡的大鼠中，从2小时开始可见相当数量强染色的Nd阳性小细胞和肿胀的曲张体，3-4小时达到最大值，并持续至24小时。这些结果表明，脊髓腹角诱导了NOS表达，包括小细胞、曲张体以及运动神经元，其在时间和程度上与脊髓Dyn神经毒性引起的运动神经元病理变化密切相关。
