Chang H M, Lue J H, Wen C Y, Shieh J Y
Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan, 100, Republic of China.
Exp Neurol. 2001 Sep;171(1):116-26. doi: 10.1006/exnr.2001.7731.
This study was aimed to determine whether axotomy coupled with hypoxia would exert a more profound effect on injury-induced neuronal nitric oxide synthase (NOS) expression. In this connection, the vagus and the hypoglossal nerves of adult rats were transected unilaterally in the same animal, and half of the operated animals were subjected to hypoxia treatment. Both the neuronal NOS immunohistochemistry and the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry were used to assess the neuronal NOS expression. The present results have shown that the number of NADPH-d/NOS-positive [NADPH-d/NOS(1)] neurons in the hypoglossal nucleus (HN) peaked at 14 days after axotomy, while that in dorsal motor nucleus of vagus (DMN) and nucleus ambiguus (NA) was progressively increased up to 60 days. The up-regulation of NADPH-d/NOS in HN and DMN was more pronounced in hypoxic than in normoxic animals, a feature that was not evident in the NA. Quantitative analysis showed that the number of surviving motoneurons in normoxic animals was significantly higher than those subjected to hypoxia at 14 days postaxotomy in HN and at all postaxotomy time points in DMN. The difference may be attributed to their different functional components. Since O2 deprivation leads to poor cellular function, the stronger expression of NADPH-d/NOS and the more drastic neuronal loss following nerve transection in the hypoxic animals compared with the controls suggest that hypoxia plays an important role in peripheral neuropathies in which NO is implicated.
本研究旨在确定轴突切断术联合缺氧是否会对损伤诱导的神经元型一氧化氮合酶（NOS）表达产生更深远的影响。就此而言，在同一只成年大鼠中单侧切断迷走神经和舌下神经，并且将一半的手术动物进行缺氧处理。采用神经元型NOS免疫组织化学和烟酰胺腺嘌呤二核苷酸磷酸黄递酶（NADPH-d）组织化学来评估神经元型NOS的表达。目前的结果表明，舌下神经核（HN）中NADPH-d/NOS阳性[NADPH-d/NOS(1)]神经元的数量在轴突切断术后14天达到峰值，而迷走神经背运动核（DMN）和疑核（NA）中的该数量则持续增加直至60天。与常氧动物相比，缺氧动物的HN和DMN中NADPH-d/NOS的上调更为明显，这一特征在NA中并不明显。定量分析表明，在轴突切断术后14天，常氧动物中存活的运动神经元数量在HN中显著高于缺氧动物，在DMN中则在轴突切断术后的所有时间点均显著高于缺氧动物。这种差异可能归因于它们不同的功能成分。由于缺氧导致细胞功能不良，与对照组相比，缺氧动物在神经切断后NADPH-d/NOS的更强表达以及更严重的神经元损失表明，缺氧在涉及NO的周围神经病变中起重要作用。
