细胞质钙离子可能参与大鼠嗜铬细胞瘤PC12细胞神经突生长的钠依赖性过程。

A possible involvement of cytoplasmic Ca2+ in sodium dependency of neurite outgrowth of rat pheochromocytoma PC12 cells.

作者信息

Koike T

出版信息

Biochim Biophys Acta. 1983 Oct 25;763(3):258-64. doi: 10.1016/0167-4889(83)90133-7.

Abstract

The effects of extracellular Na+, K+ and Cl- on neurite outgrowth of PC12 pheochromocytoma cells were studied. Nerve growth factor (NGF)-induced neurite formation was inhibited upon substitution of choline chloride for NaCl under normal culture conditions. It was found that neurite formation increased proportionately with the concentration of Na+ in medium up to 150 mM. When PC12 cells were exposed to NGF in suspension culture followed by transfer to new dishes, they showed neurite extention in response to NGF in an RNA- and protein synthesis-independent manner. Under these conditions, neurite outgrowth occurred normally in 60-150 mM Na+, whereas it decreased significantly at lower concentrations of Na+. Na+ dependency was also observed for cyclic AMP-mediated neurite formation of PC12 cells. In contrast neurite outgrowth was independent of K+ in the range 5-106 mM, suggesting that membrane potential did not play a role in this process. No alterations were observed in neurite outgrowth with Cl- replaced by NO3-, SO2-4, or 2-hydroxyethanesulfonate. Thus, extracellular Na+ plays a role in controlling neurite formation of these cells. An attempt was made to relate this effect to a decrease in cytoplasmic Ca2+ concentration monitored by a fluorescent dye sensitive to Ca2+.

摘要

研究了细胞外的Na⁺、K⁺和Cl⁻对PC12嗜铬细胞瘤细胞神经突生长的影响。在正常培养条件下，用氯化胆碱替代NaCl时，神经生长因子（NGF）诱导的神经突形成受到抑制。发现在培养基中Na⁺浓度高达150 mM时，神经突形成与Na⁺浓度成比例增加。当PC12细胞在悬浮培养中暴露于NGF后转移到新培养皿中时，它们以不依赖RNA和蛋白质合成的方式对NGF作出神经突延伸反应。在这些条件下，神经突生长在60 - 150 mM的Na⁺中正常发生，而在较低的Na⁺浓度下显著减少。PC12细胞中由环磷酸腺苷介导的神经突形成也观察到对Na⁺的依赖性。相反，在5 - 106 mM范围内神经突生长与K⁺无关，这表明膜电位在这个过程中不起作用。当Cl⁻被NO₃⁻、SO₄²⁻或2 - 羟基乙磺酸盐取代时，神经突生长没有观察到变化。因此，细胞外Na⁺在控制这些细胞的神经突形成中起作用。人们试图将这种效应与通过对Ca²⁺敏感的荧光染料监测的细胞质Ca²⁺浓度降低联系起来。