It has been recently reported by our group that GM1-oligosaccharide added to neuroblastoma cells or administered to mouse experimental model mimics the neurotrophic and neuroprotective properties of GM1 ganglioside. In addition to this, differently from GM1, GM1-oligosaccharide is not taken up by the cells, remaining solubilized into the extracellular environment interacting with cell surface proteins. Those characteristics make GM1-oligosaccharide a good tool to study the properties of the endogenous GM1, avoiding to interfere with the ganglioside natural metabolic pathway. In this study, we show that GM1-oligosaccharide administered to mice cerebellar granule neurons by interacting with cell surface induces TrkA-MAP kinase pathway activation enhancing neuron clustering, arborization and networking. Accordingly, in the presence of GM1-oligosaccharide, neurons show a higher phosphorylation rate of FAK and Src proteins, the intracellular key regulators of neuronal motility. Moreover, treated cells express increased level of specific neuronal markers, suggesting an advanced stage of maturation compared to controls. In parallel, we found that in the presence of GM1-oligosaccharide, neurons accelerate the expression of complex gangliosides and reduce the level of the simplest ones, displaying the typical ganglioside pattern of mature neurons. Our data confirms the specific role of GM1 in neuronal differentiation and maturation, determined by its oligosaccharide portion. GM1-oligosacchairide interaction with cell surface receptors triggers the activation of intracellular biochemical pathways responsible for neuronal migration, dendrites emission and axon growth.

中文翻译：

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神经节苷脂在原代神经元分化过程中：GM1-寡糖的特殊作用。

最近，我们的研究小组报道了将GM1寡糖添加到神经母细胞瘤细胞中或施用到小鼠实验模型中，可以模仿GM1神经节苷脂的神经营养和神经保护特性。除此之外，与GM1不同，GM1-寡糖不会被细胞吸收，而是溶解在与细胞表面蛋白相互作用的细胞外环境中。这些特性使GM1-寡糖成为研究内源性GM1特性的好工具，避免干扰神经节苷脂的天然代谢途径。在这项研究中，我们表明，通过与细胞表面相互作用，向小鼠小脑颗粒神经元施用GM1寡糖可诱导TrkA-MAP激酶途径活化，从而增强神经元的聚类，树状化和网络化。因此，在存在GM1寡糖的情况下，神经元显示出较高的FAK和Src蛋白（细胞内神经元运动的关键调节剂）的磷酸化率。此外，处理过的细胞表达特定神经元标记物的水平增加，表明与对照相比成熟的晚期。并行地，我们发现在存在GM1-寡糖的情况下，神经元会加速复杂神经节苷脂的表达并降低最简单神经节苷脂的水平，显示出成熟神经元的典型神经节苷脂模式。我们的数据证实了GM1在神经元分化和成熟中的特定作用，这取决于其寡糖部分。GM1-oligosacchairide与细胞表面受体的相互作用触发了负责神经元迁移的细胞内生化途径的激活，