Yu W H
Department of Cell Biology and Anatomical Sciences, City University of New York Medical School, NY 10031.
J Histochem Cytochem. 1994 Apr;42(4):451-7. doi: 10.1177/42.4.7510317.
Nitric oxide synthase (NOS), an enzyme involved in synthesis of nitric oxide (NO), has been localized in many diverse cell types. In the CNS and PNS, discrete neuron cell groups express NOS constitutively. Recent evidence indicates that NOS is inducible in neurons normally not expressing NOS. After transection of peripheral nerves, NOS expression was significantly up-regulated in the axotomized sensory ganglion cells, whereas in the corresponding motor neurons NOS was not induced unless axon regeneration was prevented and ensuing neuron death became massive. Studies on axotomy-induced NOS have been limited largely to spinal nerves, with only one reported in the vagus nerve. The aim of this study was to determine whether NOS induction in motor neurons of the brainstem after axotomy is regulated in a manner similar to that of the spinal cord. By NADPH-diaphorase histochemistry and NOS immunocytochemistry, the status of NOS in neurons of the hypoglossal nucleus, dorsal motor nucleus of the vagus, and motor nucleus of the facial nerve was examined 2 weeks after unilateral transection of the respective cranial nerves, and the results were compared with those of spinal motor neurons after transection of the sciatic nerve. NOS, undetectable in neurons of the three cranial motor nuclei of sham-operated animals, was observed in about 30-50% of neurons in the cranial motor nuclei ipsilateral to axotomy, but it was not detected in spinal motor neurons after axotomy. NOS localized in axotomized cranial motor neurons was unrelated to NOS of macrophages or endothelial cells. There was no appreciable cell loss from axotomy at this period except in the dorsal motor nucleus of the vagus, where some loss was observed. The results indicate that there is a fundamental difference in the regulation of NOS expression between motor neurons of the cranial and spinal nerves. The possible role of NOS/NO acting as cytoprotective or cytotoxic agent on injured motor neurons is discussed. Motor neurons of cranial and spinal nerves may serve as a useful model to further define the roles of NOS/NO in neurons, especially after traumatic injury.
一氧化氮合酶（NOS）是一种参与一氧化氮（NO）合成的酶，已在多种不同类型的细胞中定位。在中枢神经系统和周围神经系统中，离散的神经元细胞群组成性地表达NOS。最近的证据表明，NOS在通常不表达NOS的神经元中是可诱导的。外周神经横断后，轴突切断的感觉神经节细胞中NOS表达显著上调，而在相应的运动神经元中，除非轴突再生被阻止且随后神经元大量死亡，否则NOS不会被诱导。对轴突切断诱导的NOS的研究主要限于脊髓神经，迷走神经中仅有一项报道。本研究的目的是确定轴突切断后脑干运动神经元中NOS的诱导是否以与脊髓类似的方式受到调节。通过NADPH - 黄递酶组织化学和NOS免疫细胞化学，在相应的颅神经单侧横断2周后，检查舌下神经核、迷走神经背运动核和面神经运动核中神经元的NOS状态，并将结果与坐骨神经横断后脊髓运动神经元的结果进行比较。在假手术动物的三个颅运动核神经元中未检测到的NOS，在轴突切断同侧的颅运动核中约30 - 50%的神经元中被观察到，但在轴突切断后的脊髓运动神经元中未检测到。轴突切断的颅运动神经元中定位的NOS与巨噬细胞或内皮细胞的NOS无关。在此期间，除了在迷走神经背运动核中观察到一些细胞丢失外，轴突切断没有明显的细胞丢失。结果表明，颅神经和脊髓运动神经元中NOS表达的调节存在根本差异。讨论了NOS/NO作为细胞保护剂或细胞毒性剂对受损运动神经元的可能作用。颅神经和脊髓的运动神经元可能是进一步确定NOS/NO在神经元中的作用，特别是在创伤性损伤后的有用模型。
