Lückhoff A, Clapham D E
Department of Pharmacology, Mayo Foundation, Rochester, Minnesota 55905.
Biophys J. 1994 Jul;67(1):177-82. doi: 10.1016/S0006-3495(94)80467-9.
Depletion of intracellular calcium stores induces transmembrane Ca2+ influx. We studied Ca(2+)- and Ba(2+)-permeable ion channels in A431 cells after store depletion by dialysis of the cytosol with 10 mM BAPTA solution. Cell-attached patches of cells held at low (0.5 microM) external Ca2+ exhibited transient channel activity, lasting for 1-2 min. The channel had a slope conductance of 2 pS with 200 mM CaCl2 and 16 pS with 160 mM BaCl2 in the pipette. Channel activity quickly ran down in excised inside-out patches and was not restored by InsP3 and/or InsP4. Thapsigargin induced activation in cells kept in 1 mM external Ca2+ after BAPTA dialysis. These channels represent one Ca2+ entry pathway activated by depletion of internal calcium stores and are clearly distinct from previously identified calcium repletion currents.
细胞内钙库耗竭会诱导跨膜Ca2+内流。我们在用10 mM BAPTA溶液透析细胞质以耗尽钙库后，研究了A431细胞中Ca(2+)和Ba(2+)通透离子通道。在低（0.5 microM）细胞外Ca2+条件下的细胞进行细胞贴附式膜片钳记录时，通道呈现短暂的活性，持续1 - 2分钟。在电极液中含有200 mM CaCl2时，该通道的斜率电导为2 pS，含有160 mM BaCl2时为16 pS。在切除的内面向外膜片中，通道活性迅速衰减，且不能被InsP3和/或InsP4恢复。在BAPTA透析后，毒胡萝卜素能诱导处于1 mM细胞外Ca2+环境中的细胞激活这些通道。这些通道代表了一种由内部钙库耗竭激活的Ca2+内流途径，明显不同于先前鉴定的钙补充电流。
