LA-N-1细胞的膜去极化。乳酸菌毒素的作用依赖于Ca(2+)-和Na(+)-。

G Sorrentino, M R Monsurrõ, I N Singh, J N Kanfer
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引用次数: 4

摘要

我们使用比索醇作为电位敏感荧光染料,研究了离子组成对LA-N-1人神经母细胞瘤细胞膜电位的影响。研究了K+、瓦巴因、缬草碱和乳酸菌毒素诱导细胞膜去极化的能力。当K+离子浓度从10 ~ 50 mM增加时,双索醇荧光呈剂量依赖性增加,完全不依赖于Na+和Ca2+。一种Na+, K(+)- atp酶抑制剂(5 mM) Ouabain未能诱导膜去极化。缬曲定(40和100微米)是一种Na+通道激活剂,仅在10微克的蝎毒存在下才降低膜电位。Maitotoxin (MTX)浓度从3 ~ 10 ng/mL呈剂量依赖性地去极化LA-N-1细胞,并通过荧光探针fura-2监测细胞内游离钙的快速持续增加。mtx诱导的去极化和胞质游离钙浓度的增加依赖于胞外Ca2+离子。另一方面,尽管只是部分地,但Na+离子似乎也与MTX效应有关,因为阻断河豚毒素(TTX)敏感的电压操作Na+通道和去除Na+离子都能够减少去极化。总之,我们的数据表明,MTX对LA-N-1细胞的去极化作用是Ca(2+)和Na(+)依赖的,尽管后者只是部分依赖,并且这种作用依赖于Ca2+可能通过电压不敏感的钙进入系统流入细胞。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Membrane depolarization in LA-N-1 cells. The effect of maitotoxin is Ca(2+)- and Na(+)-dependent.

We investigated the influence of ion compositions on the membrane potential in LA-N-1 human neuroblastoma cells using bisoxonol as a potential-sensitive fluorescent dye. The ability of K+, ouabain, veratridine, and maitotoxin to induce membrane depolarization was evaluated. Increasing concentrations of K+ ions from 10 to 50 mM caused a dose-dependent increase of bisoxonol fluorescence, which was completely independent on Na+ and Ca2+. Ouabain (5 mM), an inhibitor of the Na+, K(+)-ATPase, failed to induce membrane depolarization. Veratridine (40 and 100 microM), a Na+ channel activator, only in the presence of 10 micrograms of Leiurus scorpion venom reduced the membrane potential. Maitotoxin (MTX) from 3 to 10 ng/mL depolarized LA-N-1 cells in a dose-dependent manner, and produced a rapid and sustained increase of intracellular free calcium monitored by means of fluorescent probe fura-2. The MTX-induced depolarization and the increase in cytosolic free calcium concentration were dependent on extracellular Ca2+ ions. On the other hand, Na+ ions also seem to be, although only partially, implicated in the MTX effects, since both the blockade of tetrodotoxin (TTX)-sensitive voltage-operated Na+ channels and the removal of Na+ ions were able to reduce the depolarization. In conclusion, our data indicate that the depolarizing action of MTX on LA-N-1 cells is Ca(2+)- and Na(+)-dependent, although the latter only partially, and that this effect is dependent on Ca2+ influx into the cells likely through a voltage-insensitive calcium-entry system.

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