Morán J, Pasantes-Morales H
Institute of Cell Physiology, National University of Mexico, Mexico City.
J Neurosci Res. 1991 Aug;29(4):533-7. doi: 10.1002/jnr.490290414.
Mouse cerebellar granule neurons and astrocytes grown in the presence of 2 mM guanidinoethane sulfonate (GES) exhibited a progressive and rapid decrease in taurine concentration. A reduction of 20% was observed as early as 1 hr after exposure to GES and the loss of cell taurine continued until the taurine pool was reduced by about 90%. This remaining taurine persisted without further decrease even after 3 weeks of exposure to GES. Taurine reduction caused by GES was similar in both types of cells. The effect of GES was dose-dependent, with significant decreases in taurine levels already detected at 100 microM. It was selective for taurine, since none of the other free amino acids were affected. Taurine depletion induced by GES was totally reversible. Intracellular taurine was not mobilized by GES. Taurine uptake in both astrocytes and granule neurons, examined at the taurine concentration present in the culture medium, was practically abolished by 2 mM GES. This approach represents an in vitro model of taurine depletion that may be useful to investigate the cell abnormalities responsible for the failure of differentiation and migration of granule cells and astrocytes observed in taurine-deficient cats.
在含有2 mM胍基乙磺酸盐(GES)的条件下培养的小鼠小脑颗粒神经元和星形胶质细胞,其牛磺酸浓度呈现出逐渐且快速的下降。早在暴露于GES 1小时后就观察到牛磺酸浓度降低了20%,并且细胞内牛磺酸的损失持续进行,直到牛磺酸池减少约90%。即使在暴露于GES 3周后,剩余的牛磺酸浓度也保持不变,不再进一步降低。GES引起的牛磺酸减少在这两种细胞类型中相似。GES的作用呈剂量依赖性,在100 microM时就已检测到牛磺酸水平显著下降。它对牛磺酸具有选择性,因为其他游离氨基酸均未受到影响。GES诱导的牛磺酸耗竭是完全可逆的。GES不会动员细胞内的牛磺酸。在培养基中存在的牛磺酸浓度下检测发现,2 mM GES几乎完全消除了星形胶质细胞和颗粒神经元对牛磺酸的摄取。这种方法代表了一种牛磺酸耗竭的体外模型,可能有助于研究导致在牛磺酸缺乏的猫中观察到的颗粒细胞和星形胶质细胞分化及迁移失败的细胞异常情况。