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首页> 外文期刊>Life sciences >Effects of ethanol on phosphoinositide hydrolysis and muscarinic acetylcholine receptor number in SH-SY5Y cells.
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Effects of ethanol on phosphoinositide hydrolysis and muscarinic acetylcholine receptor number in SH-SY5Y cells.

机译：乙醇对SH-SY5Y细胞磷酸肌醇水解和毒蕈碱型乙酰胆碱受体数目的影响。

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Previous studies suggest that the effects of ethanol on carbachol-stimulated I(1,4,5)P3 formation and on the number of mAChRs may be independent of each other. The aim of this work was to further study this hypothesis. Human neuroblastoma SH-SY5Y cells were used as a model system. Acute exposure of the cells to 100 mM ethanol induced a decrease in [3H]N-methylscopolamine ([3H]NMS) binding at 30 seconds which was of lower magnitude and of shorter duration than the previously described ethanol-induced inhibition of the peak of carbachol-stimulated I(1,4,5)P3 formation. Long-term ethanol treatment of the cells induced a time- and concentration-dependent increase in [3H]NMS binding. Three hours of 100 mM ethanol treatment were sufficient to increase the number of mAChRs at the cell surface but these receptors were not immediately functionally active, suggesting that they may be newly synthesized. Furthermore, the ethanol-induced potentiation of carbachol-stimulated I(1,4,5)P3 formation, after two days, was, for all ethanol concentrations tested, of higher magnitude than the ethanol-induced increase in mAChR number. Together, these data indicate that both acute and chronic ethanol-induced changes in carbachol-stimulated I(1,4,5)P3 formation may not only be explained by changes in mAChR density at the cell surface but may rather be the consequence of actions of ethanol down-stream of the receptor.
机译：先前的研究表明，乙醇对卡巴胆碱刺激的I（1,4,5）P3的形成以及mAChR数量的影响可能彼此独立。这项工作的目的是进一步研究该假设。人类神经母细胞瘤SH-SY5Y细胞用作模型系统。将细胞急性暴露于100 mM乙醇会导致[3H] N-甲基东pol碱（[3H] NMS）结合在30秒时减少，其幅度和持续时间均比先前描述的乙醇诱导的对CAMP峰的抑制要低。卡巴胆碱刺激的I（1,4,5）P3形成。细胞的长期乙醇处理诱导了[3H] NMS结合的时间依赖性和浓度依赖性增加。 100 mM乙醇处理3小时足以增加细胞表面mAChR的数量，但这些受体并未立即发挥功能活性，表明它们可能是新合成的。此外，对于所有测试的乙醇浓度，两天后，乙醇诱导的卡巴胆碱刺激的I（1,4,5）P3形成的增强幅度均高于乙醇诱导的mAChR数量增加幅度。总之，这些数据表明，乙醇引起的急性和慢性乙醇诱导的I（1,4,5）P3形成的变化不仅可以通过细胞表面mAChR密度的变化来解释，而且可能是作用的结果受体下游的乙醇。

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