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轴突切断术和传入神经阻滞对大鼠颈上神经节神经元中神经丝蛋白磷酸化依赖性抗原性的影响。

The effect of axotomy and deafferentation on phosphorylation dependent antigenicity of neurofilaments in rat superior cervical ganglion neurons.

作者信息

Shaw G, Winialski D, Reier P

机构信息

Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610.

出版信息

Brain Res. 1988 Sep 20;460(2):227-34. doi: 10.1016/0006-8993(88)90367-8.

Abstract

Previous immunocytochemical studies have shown immunological differences between neurofilaments in axons and those in dendrites and perikarya of many mature neuron types: it is now known that non-phosphorylated epitopes are normally seen in cell bodies and dendrites of mature neurons, whereas phosphorylated epitopes are observed in axons. Further studies on a variety of cell types have shown that phosphorylated epitopes are induced in the cell-body associated neurofilaments following axotomy, and we show here that comparable changes are observed in axotomized rat superior cervical ganglion neurons (SCG). We have also observed that preganglionic section induces similar changes in the levels of neurofilament phosphorylation, so that phosphorylated epitopes become visible in the cell bodies and dendrites of denervated neurons. The changes in this case appear more slowly and are accompanied by the appearance of punctate nuclear staining detectable with phosphorylation sensitive neurofilament antibodies. The acquisition of these staining patterns by both the axotomized and denervated SCG cells proved to be reversible, so that after 10-12 days no neurons in either experimental group exhibited perikaryal phosphorylated epitopes. These results indicate that changes in the level of neurofilament phosphorylation are not only associated with neuronal damage, but can also be induced by deafferentation.

摘要

先前的免疫细胞化学研究表明,在许多成熟神经元类型的轴突、树突和胞体中的神经丝之间存在免疫学差异:现在已知非磷酸化表位通常见于成熟神经元的细胞体和树突中,而磷酸化表位则见于轴突中。对多种细胞类型的进一步研究表明,轴突切断后,在与细胞体相关的神经丝中可诱导出磷酸化表位,并且我们在此表明,在切断轴突的大鼠颈上神经节神经元(SCG)中也观察到了类似的变化。我们还观察到,节前切断会诱导神经丝磷酸化水平发生类似变化,从而使去神经支配神经元的细胞体和树突中可见磷酸化表位。在这种情况下,变化出现得较慢,并伴有可被磷酸化敏感神经丝抗体检测到的点状核染色的出现。切断轴突和去神经支配的SCG细胞获得这些染色模式被证明是可逆的,因此在10 - 12天后,两个实验组中均没有神经元表现出胞体磷酸化表位。这些结果表明,神经丝磷酸化水平的变化不仅与神经元损伤有关,还可由传入神经阻滞诱导产生。

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