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解离的胎鼠中脑无血清细胞培养物中神经元的发育与存活:II. 神经节苷脂的调节作用

Development and survival of neurons in dissociated fetal mesencephalic serum-free cell cultures: II. Modulatory effects of gangliosides.

作者信息

Leon A, Dal Toso R, Presti D, Benvegnù D, Facci L, Kirschner G, Tettamanti G, Toffano G

机构信息

Fidia Neurobiological Research Laboratories, Abano Terme, Italy.

出版信息

J Neurosci. 1988 Mar;8(3):746-53. doi: 10.1523/JNEUROSCI.08-03-00746.1988.

Abstract

This paper analyzes the effects of exogenously supplied GM1 on the development, i.e., specific neurotransmitter uptake capability and survival, of the dopaminergic neurons present in fetal mouse-dissociated mesencephalic cells. Exogenous GM1, but not asialo-GM1, sialic acid, or the oligosaccharide chain of GM1, enhances in a time- and concentration-dependent manner the specific 3H-dopamine uptake (increase of the apparent Vmax and decrease of the apparent Km value) and the long-term survival of the dopaminergic neurons. The GM1 effects on the behavior of the dopaminergic neurons require the presence of cell-derived neuronotrophic influences present within the culture system and are associated with an increase in the response of the cells to the trophic influences. GM1 effects are not limited to dopaminergic neurons, and depend on the stable association of the ganglioside molecule with the cells. It is suggested that GM1 is not a trophic agent per se, but rather potentiates neuronotrophic activities and/or exerts independent influences to which neurons respond only if appropriately supported.

摘要

本文分析了外源性给予的GM1对胎鼠中脑解离细胞中多巴胺能神经元发育的影响,即对其特定神经递质摄取能力和存活的影响。外源性GM1而非去唾液酸GM1、唾液酸或GM1的寡糖链,以时间和浓度依赖性方式增强了特定的3H-多巴胺摄取(表观Vmax增加和表观Km值降低)以及多巴胺能神经元的长期存活。GM1对多巴胺能神经元行为的影响需要培养系统中存在细胞源性神经营养影响,并且与细胞对营养影响的反应增加有关。GM1的作用不仅限于多巴胺能神经元,且取决于神经节苷脂分子与细胞的稳定结合。有人提出,GM1本身并非一种营养因子,而是增强了神经营养活性和/或施加了独立影响,而神经元只有在得到适当支持时才会对这些影响做出反应。

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