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神经生长因子可刺激体外培养的成年听觉神经元的神经突再生,但不能促进其存活。

Nerve growth factor stimulates neurite regeneration but not survival of adult auditory neurons in vitro.

作者信息

Lefebvre P P, Van de Water T R, Staecker H, Weber T, Galinović-Schwartz V, Moonen G, Ruben R J

机构信息

Department of Otolaryngology and Audiophonology, University of Liege, Belgium.

出版信息

Acta Otolaryngol. 1992;112(2):288-93. doi: 10.1080/00016489.1992.11665420.

Abstract

Injury to either the peripheral or central nervous system results in the accumulation of growth factors at the wound site. Some of these growth factors have been shown to participate in the neural repair process. Adult auditory neurons grown in dissociated spiral ganglion cell cultures are injured (i.e. bilateral axotomy) as a result of the initial preparation of these cultures. Therefore, cell cultures of dissociated spiral ganglia provide a model for the study of repair processes of adult auditory neurons (e.g. effects of exogenous growth factors on the process of neuritogenesis by injured neurons). Auditory neurons do not survive in these dissociated ganglion cell cultures when only exogenous NGF is added to the defined culture medium. Previous work has identified substrate bound basic fibroblast growth factor (bFGF) as a survival factor for adult auditory neurons in vitro. Auditory neurons cultured on substrate bound bFGF also do not show increased survival in response to the addition of increasing concentrations of nerve growth factor (NGF) to the defined medium. This is in sharp contrast to the pronounced neurite outgrowth-promoting effects (concentration dependent) observed when exogenous NGF is added to adult auditory neurons cultured on substrate bound bFGF. We propose that several neuronotrophic factors (e.g. TGFB1, bFGF, NGF and other neurotrophins) are active in the spiral ganglions' response to injury. Several of these growth factors (i.e. bFGF, NGF) act in cooperation to promote the regeneration or repair of severed or traumatized neuritic processes.

摘要

外周或中枢神经系统损伤会导致伤口部位生长因子的积累。其中一些生长因子已被证明参与神经修复过程。在解离的螺旋神经节细胞培养物中生长的成年听觉神经元,由于这些培养物的初始制备而受到损伤(即双侧轴突切断)。因此,解离的螺旋神经节细胞培养物为研究成年听觉神经元的修复过程提供了一个模型(例如外源性生长因子对受损神经元神经突形成过程的影响)。当仅向限定培养基中添加外源性神经生长因子(NGF)时,听觉神经元在这些解离的神经节细胞培养物中无法存活。先前的研究已确定底物结合的碱性成纤维细胞生长因子(bFGF)是成年听觉神经元在体外的存活因子。在底物结合的bFGF上培养的听觉神经元,在向限定培养基中添加浓度不断增加的神经生长因子(NGF)时,也未显示出存活率增加。这与向在底物结合的bFGF上培养的成年听觉神经元添加外源性NGF时观察到的明显的(浓度依赖性)促神经突生长效应形成鲜明对比。我们提出几种神经营养因子(例如转化生长因子β1、bFGF、NGF和其他神经营养蛋白)在螺旋神经节对损伤的反应中起作用。这些生长因子中的几种(即bFGF、NGF)协同作用,促进切断或受损神经突的再生或修复。

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