Klosen P, Anderton B H, Brion J P, van den Bosch de Aguilar P
Laboratoire de Biologie Cellulaire, Université Catholique de Louvain, Belgium.
Brain Res. 1990 Sep 3;526(2):259-69. doi: 10.1016/0006-8993(90)91230-e.
The axon reaction in the central nervous system was studied using a monoclonal antibody to phosphorylated neurofilaments. Axotomy was performed by cutting the nigrostriatal pathway. We were able to show that phosphorylated epitopes of neurofilaments, that are usually restricted to axons, could be detected in the perikarya and dendrites of axotomized neurons as early as 3 days postlesion. These neurons remained labelled up to 17 days after axotomy and in some cases even up to 6 weeks. The cytoplasmic changes appearing in the lesioned neurons 8 days after axotomy seem to indicate that these neurons will probably degenerate or survive only in an atrophied, non-functional state as they are unable to regenerate their sectioned axon. Neurochemical lesions, using the neurotoxin 6-OH-dopamine, were performed to establish whether this reaction of perikaryal neurofilament phosphorylation may be a non-specific phenomenon accompanying neuronal degeneration or injury. Although cell loss was important, no labelled neurons could be observed following 6-OH-dopamine treatment. These results indicate that the induction of perikaryal neurofilament phosphorylation is a response to selective types of neuronal injury and concerns selective neuronal populations.
利用针对磷酸化神经丝的单克隆抗体，对中枢神经系统中的轴突反应进行了研究。通过切断黑质纹状体通路来进行轴突切断术。我们能够证明，通常局限于轴突的神经丝磷酸化表位，在损伤后3天就能够在轴突切断的神经元的胞体和树突中被检测到。这些神经元在轴突切断后长达17天一直保持标记，在某些情况下甚至长达6周。轴突切断后8天，受损神经元中出现的细胞质变化似乎表明，这些神经元可能会退化，或者仅在萎缩、无功能的状态下存活，因为它们无法再生被切断的轴突。使用神经毒素6-羟基多巴胺进行神经化学损伤，以确定这种胞体神经丝磷酸化反应是否可能是伴随神经元变性或损伤的非特异性现象。尽管细胞损失很严重，但在6-羟基多巴胺处理后未观察到标记的神经元。这些结果表明，胞体神经丝磷酸化的诱导是对选择性类型神经元损伤的一种反应，并且涉及选择性神经元群体。
