Istin M, Kirschner L B
J Gen Physiol. 1968 Apr;51(4):478-96. doi: 10.1085/jgp.51.4.478.
Mantles from freshwater clams develop potential differences (PD's) between the two surfaces when they are bathed in vitro with artificial saline solutions. The magnitude and polarity of the PD is dependent on [Ca(2+)] in the solution bathing the mantle's shell surface. When the solutions are gassed with 5% CO(2) in oxygen, the PD is in the range 25 to 50 mv, shell side positive. It decreases if [Ca(2+)] in the shell solution is elevated. The concentration dependence is logarithmic with a slope of about -27 mv per 10-fold change in [Ca(2+)], slightly less than predicted by the Nernst equation for a membrane acting as a calcium electrode. Analysis of the electrical behavior both in intact mantles and in isolated epithelia indicates that most of the PD develops across the external membranes of epithelial cells on the shell side. There is no evidence that an active calcium transport system is involved in electrogenesis, and a model based on calcium diffusion across a selectively permeable membrane can explain existent data. If CO(2) is absent, the mantle PD is very small (2-10 mv), but still sensitive to change in external [Ca(2+)]. It is proposed that CO(2) alters intracellular pH, thereby changing the equilibrium between a large store of nonionized calcium and [Ca(2+)] in the cells. A role for carbonic anhydrase in the CO(2) effect is suggested by the action of a specific inhibitor of this enzyme. The diffusion model predicts that increasing ionized calcium should increase the PD as is actually observed. Some implications of this system for the physiology of calcium movement in vivo are discussed.
淡水蛤蜊的外套膜在体外浸泡于人工盐溶液时，两个表面之间会产生电位差（PD）。PD的大小和极性取决于浸泡在外套膜壳表面的溶液中的[Ca(2+)]。当溶液用含5% CO(2)的氧气曝气时，PD在25至50毫伏范围内，壳侧为正。如果壳溶液中的[Ca(2+)]升高，PD会降低。浓度依赖性呈对数关系，[Ca(2+)]每10倍变化时斜率约为-27毫伏，略小于作为钙电极的膜的能斯特方程预测值。对完整外套膜和分离上皮细胞的电行为分析表明，大部分PD是在壳侧上皮细胞的外膜上产生的。没有证据表明有活性钙转运系统参与电生成，基于钙在选择性渗透膜上扩散的模型可以解释现有数据。如果没有CO(2)，外套膜PD非常小（2 - 10毫伏），但仍对外部[Ca(2+)]的变化敏感。有人提出，CO(2)会改变细胞内pH，从而改变细胞内大量非离子化钙与[Ca(2+)]之间的平衡。该酶的特异性抑制剂的作用表明碳酸酐酶在CO(2)效应中起作用。扩散模型预测，增加离子化钙应会增加PD，这与实际观察到的情况一致。本文讨论了该系统对体内钙运动生理学的一些影响。
