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坐骨神经损伤后及再生过程中,神经生长因子(NGF)受体介导的轴突对NGF摄取及逆向运输的减少。

NGF receptor-mediated reduction in axonal NGF uptake and retrograde transport following sciatic nerve injury and during regeneration.

作者信息

Raivich G, Hellweg R, Kreutzberg G W

机构信息

Department of Neuromorphology, Max-Planck-Institute for Psychiatry, Martinsried, Germany.

出版信息

Neuron. 1991 Jul;7(1):151-64. doi: 10.1016/0896-6273(91)90083-c.

Abstract

Injury to the rat sciatic nerve leads to the induction of nerve growth factor (NGF) receptors on the denervated Schwann cells and their disappearance on the regenerating axons of the axotomized, normally NGF-sensitive sensory and sympathetic neurons. This disappearance in the axonal expression and retrograde transport of NGF receptors is associated with a similarly dramatic reduction in the axonal uptake and retrograde transport of NGF following axotomy and during regeneration. In view of the massive NGF synthesis occurring in the injured nerve, these results suggest that, while sensory and sympathetic neurons are the primary targets of NGF in the normal peripheral nervous system, the denervated Schwann cells may become its primary target in the aftermath of nerve injury.

摘要

大鼠坐骨神经损伤会导致去神经支配的施万细胞上诱导出神经生长因子(NGF)受体,而在轴突切断的、正常情况下对NGF敏感的感觉神经元和交感神经元的再生轴突上,这些受体会消失。轴突切断后及再生过程中,NGF受体在轴突中的表达及逆行运输的消失,与轴突对NGF的摄取及逆行运输同样显著减少有关。鉴于损伤神经中发生大量NGF合成,这些结果表明,虽然感觉神经元和交感神经元在正常外周神经系统中是NGF的主要靶点,但在神经损伤后,去神经支配的施万细胞可能会成为其主要靶点。

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