Motor neuronal damage due to diseases, traumatic insults or de-afferentation of the spinal cord is often incurable because of poor intrinsic regenerative capacity. Hence, medical basic research has to provide a better understanding of development-/regeneration-related cellular processes as only way to develop new and successful therapeutic strategies. Here, we investigated the neuronal differentiation of the NSC-34 hybrid cell line, which is an accepted model for spinal cord motor neurons. Their differentiation was stimulated by switching from normal to differentiation medium and by supplementation with palmitic and oleic acid. To characterize neuro-differentiation of NSC-34 cells, expression of nicotinic acetylcholine receptor alpha 4, NGF p75 receptor, IGF I alpha receptor, glutaminase, NCAM L1, ADAM10 and myelin basic protein as well as activation of mitochondria were analyzed. Both switch from normal to differentiation medium and fatty acid application stimulated NSC-34 differentiation. Differentiation was characterized by diminishing expression of the nicotinic acetylcholine receptor alpha 4 and enhancing expression of the NGF receptor p75, of glutaminase, of NCAM L1 and it’s partially transformation from the cell surface into the cell. Fatty acid intervention stabilized the expression of the nicotinic acetylcholine receptor alpha 4, diminished the expression of the NGF receptor p75, consolidated the expression profile of NCAM L1, and intensified the expression of the relevant for NCAM L1 cleavage ADAM10. However, NCAM L1 cleavage itself was unaffected by fatty acid intervention, as was the differentiation-relevant activation of mitochondria and their transformation into neuronal filopodia.

由于固有的再生能力差，通常无法治愈由于疾病，外伤性损伤或脊髓失能引起的运动神经元损害。因此，医学基础研究必须更好地了解与发育/再生有关的细胞过程，这是开发新的成功治疗策略的唯一途径。在这里，我们研究了NSC-34杂交细胞系的神经元分化，这是脊髓运动神经元的公认模型。从正常培养基转换为分化培养基并补充棕榈酸和油酸可刺激它们的分化。为了表征NSC-34细胞的神经分化，需要表达烟碱乙酰胆碱受体α4，NGF p75受体，IGF Iα受体，谷氨酰胺酶，NCAM L1，分析了ADAM10和髓鞘碱性蛋白以及线粒体的活化。两者均从正常培养基转变为分化培养基，脂肪酸的应用刺激了NSC-34的分化。分化的特征是烟碱型乙酰胆碱受体α4的表达减少，而NGF受体p75，谷氨酰胺酶，NCAM L1的表达增强，并且它从细胞表面部分转化为细胞。脂肪酸干预稳定了烟碱乙酰胆碱受体α4的表达，减少了NGF受体p75的表达，巩固了NCAM L1的表达谱，并增强了与NCAM L1裂解ADAM10相关的表达。但是，NCAM L1裂解本身不受脂肪酸干预的影响，