Local nitric oxide production in viral and autoimmune diseases of the central nervous system.

Because of the short half-life of NO, previous studies implicating NO in central nervous system pathology during infection had to rely on the demonstration of elevated levels of NO synthase mRNA or enzyme expression or NO metabolites such as nitrate and nitrite in the infected brain. To more definitively investigate the potential causative role of NO in lesions of the central nervous system in animals infected with neurotropic viruses or suffering from experimental allergic encephalitis, we have determined directly the levels of NO present in the central nervous system of such animals. Using spin trapping of NO and electron paramagnetic resonance spectroscopy, we confirm here that copious amounts of NO (up to 30-fold more than control) are elaborated in the brains of rats infected with rabies virus or borna disease virus, as well as in the spinal cords of rats that had received myelin basic protein-specific T cells.

由于一氧化氮（NO）的半衰期较短，既往针对感染期间一氧化氮在中枢神经系统病理过程中作用的研究，不得不依赖于检测感染脑组织内一氧化氮合酶（NO synthase）信使核糖核酸（mRNA）的表达水平、酶表达情况，或是一氧化氮代谢物（如硝酸盐、亚硝酸盐）的升高幅度。为更明确地探究一氧化氮在嗜神经病毒感染动物，或罹患实验性变应性脑炎的动物的中枢神经系统损伤中的潜在致病作用，我们直接测定了此类动物中枢神经系统内的一氧化氮水平。本研究采用自旋捕获（spin trapping）联合电子顺磁共振波谱法（electron paramagnetic resonance spectroscopy），证实狂犬病病毒（rabies virus）或博尔纳病病毒（borna disease virus）感染的大鼠脑组织，以及接受了髓鞘碱性蛋白（myelin basic protein）特异性T细胞的大鼠脊髓中，均可产生大量一氧化氮，其水平最高可达对照组的30倍。