Estacion M, Nguyen H B, Gargus J J
Department of Physiology and Biophysics, University of California, Irvine 92717, USA.
Am J Physiol. 1996 Apr;270(4 Pt 1):C1145-52. doi: 10.1152/ajpcell.1996.270.4.C1145.
The shellfish poison maitotoxin causes the irreversible opening of nonselective cation channels in mouse L cell fibroblasts, consistent with the action of this toxin in other cell types and the previously demonstrated existence of 28-pS voltage-insensitive nonselected cation channels that are activated by platelet-derived growth factor in these cells. Toxin-induced opening of these nonselective cation channels led to increases of intracellular calcium and secondary activation of calcium-activated potassium channel. These effects were completely dependent on influx of extracellular calcium, supporting the conclusion that the maitotoxin-activated nonselective cation channels are permeable to calcium as well as to sodium and potassium. The implication of this finding is that calcium signaling through this channel underlies its links into the growth factor response.
贝类毒素刺尾鱼毒素可导致小鼠L细胞成纤维细胞中的非选择性阳离子通道不可逆开放，这与该毒素在其他细胞类型中的作用一致，并且此前已证明在这些细胞中存在由血小板衍生生长因子激活的28皮秒电压不敏感非选择性阳离子通道。毒素诱导这些非选择性阳离子通道开放导致细胞内钙增加以及钙激活钾通道的继发性激活。这些效应完全依赖于细胞外钙的内流，支持了刺尾鱼毒素激活的非选择性阳离子通道对钙以及钠和钾都有通透性的结论。这一发现的意义在于，通过该通道的钙信号传导是其与生长因子反应联系的基础。
