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辣根过氧化物酶在横断轴突中的逆行运输。3. 进入损伤轴突并随后定位于核周体。

Retrograde transport of horseradish peroxidase in transected axons. 3. Entry into injured axons and subsequent localization in perikaryon.

作者信息

Kristensson K, Olsson Y

出版信息

Brain Res. 1976 Oct 15;115(2):201-13. doi: 10.1016/0006-8993(76)90507-2.

Abstract

Horseradish peroxidase (HRP) applied to crushed mouse sciatic nerves diffused through the damaged perineurium into the endoneurium. In the injured area, HRP passed into damaged myelinated and unmyelinated axons forming columns of reaction product, which extended for several millimeters proximally to the lesion. Ultrastructurally, HRP adhered to the inner surface of the axoplasm and to the surfaces of neurotubules and neurofilaments in such columns. At more proximal levels axons contained HRP in vesicular and tubular organelles and, later, nerve cell bodies of the corresponding spinal ganglia showed HRP, accumulation in cytoplasmic vesicles, cup-shaped bodies, multivesicular bodies and tubules of agranular endoplasmic reticulum. Markedly less HRP reached neurons in the spinal ganglia when applied to the nerve 30 or 60 min after the crush. After such time intervals solid HRP containing axons were also less frequently observed. Conceivably, HRP enters crushed axons momentarily after a crush as an injured cell reaction. Subsequently it is incorporated into organelles higher up in the axons, from where retrograde transport to the perikaryon will fellow. This phenomenon of a sudden non-specific influx of exogenous macromolecules into axotomized neurons and their subsequent transport to the perikaryon might be relevant for development of certain biochemical and morphological responses, e.g. lysosomal alterations, of the neuron to an axonal injury.

摘要

将辣根过氧化物酶(HRP)应用于挤压损伤的小鼠坐骨神经,它会通过受损的神经束膜扩散到神经内膜。在损伤区域,HRP进入受损的有髓和无髓轴突,形成反应产物柱,该反应产物柱向损伤部位近端延伸数毫米。在超微结构上,HRP附着于这些柱内轴浆的内表面以及神经微管和神经丝的表面。在更靠近近端的水平,轴突在囊泡状和管状细胞器中含有HRP,随后,相应脊髓神经节的神经细胞体显示HRP积聚在细胞质囊泡、杯状体、多泡体和无颗粒内质网的小管中。在挤压后30或60分钟将HRP应用于神经时,到达脊髓神经节神经元的HRP明显减少。在这样的时间间隔后,含有HRP的实心轴突也较少见。可以想象,挤压后HRP作为一种损伤细胞反应会瞬间进入挤压损伤的轴突。随后它被纳入轴突中更高位置的细胞器,从那里逆行运输到胞体。这种外源性大分子突然非特异性流入轴突切断的神经元并随后运输到胞体的现象可能与神经元对轴突损伤的某些生化和形态学反应(例如溶酶体改变)的发展有关。

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