乙醇对颈上神经元细胞内外钙信号的双重作用

Effects of Extracellular Calcium Release by Ethanol in Sympathetic Dysfunction

目的:探讨乙醇对原代培养颈上神经节神经元(SCGs)细胞质钙稳态的影响。方法:分散、培养新生12 h内大鼠SCGs,应用激光共聚焦显微技术,观察不同浓度乙醇对SCGs细胞质Ca2+浓度([Ca2+]i)的作用。结果:KCl及钙离子载体A23187所诱发的[Ca2+]i增高,可被乙醇(100 mmol/L)显著抑制,但是乙醇(30,100,600 mmol/L)自身却可浓度依赖性增加[Ca2+]i,并且使用无Ca2+外液和氯化镉对该增加作用无影响。结论:乙醇可抑制细胞外Ca2+内流,同时增加细胞质[Ca2+]i,来源可能是胞内钙库的释放。

Objective： To investigate the interference of calcium homeostasis by ethanol on the primary cultured superior cervical ganglion neurons （SCGs）. Methods： SCGs were dissociated enzymati- caly and cultured from the rats within 12 hours postnatal, and the effect of different concentration of ethanol on cytoplasmic calcium concentration （~Ca 2＋ ]i） in cultured SCGs was measured by la- ser scanning confocal microscopy. Results： Ethanol （100 mmol/L） significantly inhibited[Ca2＋]ii increments evoked by KC1 from 1. 725±-0. 159 to 1. 156±0. 135 （F/F0）. Inhibition of A23187-in- duced [Ca2＋]i increment by ethanol （100 mmol/L） was significant from 2. 232 ＋0. 015 to 1. 263 ± 0.047 （F/F0）. Whereas the ethanol alone could increase basal [Ca2＋]i in a dose-dependent man- ner, even when extracellular Ca2＋ removed or cadmium chloride applied. Conclusion： Extracellu- lar calcium influx both through voltage-dependent calcium channel and ionophore channel are in- hibited by ethanol. But the ethanol alone could increase basal [Ca2＋]i, which suggests the aug- ment of [Ca2＋]i comes from intraeellular calcium pools.