Foskett J K, Machen T E
J Membr Biol. 1985;85(1):25-35. doi: 10.1007/BF01872003.
We have utilized the vibrating probe technique to examine transport by individual chloride cells in the short-circuited fish opercular epithelium. Variability in the steady state and in response to rapid perturbations, including fast-acting hormones and ion replacement, was analyzed. Negative short-circuit currents, corresponding to chloride secretion, were associated with the apical crypts of all but five of 386 chloride cells sampled. Average chloride cell short-circuit current and conductance were 2.7 +/- 0.1 nA and 87.7 +/- 3.8 nS, respectively, or 19 mA cm-2 and 620 mS cm-2 (resistance = 1.6 omega cm2) when normalized to apical crypt surface area. Exposure to 1 microM epinephrine rapidly inhibited the tissue short-circuit current by inhibiting the current pumped by all chloride cells, i.e. all chloride cells have adrenergic receptors. The time course of inhibition for each cell mirrored that of the whole tissue. Reversal of epinephrine inhibition of the tissue short-circuit current by glucagon and phosphodiesterase inhibition was by reversal of epinephrine's inhibition of individual chloride cells, and not by turning on cells which were previously inactive or uninhibited, or by stimulating nonchloride cells. A great amount of variability existed among chloride cells in the ability of these agents to reverse epinephrine-inhibited current. Likewise, considerable variability in the response of chloride cell conductance to these perturbations was observed, and in many instances a clear dissociation between current and conductance was noted. In the steady state, variability among cells in a single tissue always defined a linear relationship between chloride cell current and conductance with zero-current conductance intercept at zero. Equivalent circuit modeling indicates that the leak conductance of chloride cells within a single tissue always contributes the same proportion to the total individual chloride cell conductance, such that the ratio between the conductances of the active and leak pathways of chloride cells is constant. The leak pathway is almost certainly dominated by a sodium-selective paracellular pathway. The results suggest that these cells control the permeability of their paracellular pathway. A possible mechanism for this control is discussed.
我们利用振动探针技术研究了短路状态下鱼鳃上皮单个氯化物细胞的物质运输情况。分析了稳态以及对包括速效激素和离子置换在内的快速扰动的反应中的变异性。对应于氯化物分泌的负短路电流与所采样的386个氯化物细胞中除5个之外的所有细胞的顶端隐窝相关。平均氯化物细胞短路电流和电导分别为2.7±0.1 nA和87.7±3.8 nS，当按顶端隐窝表面积归一化时分别为19 mA cm-2和620 mS cm-2（电阻=1.6Ω cm2）。暴露于1μM肾上腺素会通过抑制所有氯化物细胞所泵出的电流来迅速抑制组织短路电流，即所有氯化物细胞都有肾上腺素能受体。每个细胞的抑制时间进程与整个组织的相似。胰高血糖素和磷酸二酯酶抑制作用使肾上腺素对组织短路电流的抑制作用逆转，是通过逆转肾上腺素对单个氯化物细胞的抑制作用实现的，而不是通过激活先前无活性或未受抑制的细胞，也不是通过刺激非氯化物细胞。这些药剂逆转肾上腺素抑制电流的能力在氯化物细胞之间存在很大变异性。同样，观察到氯化物细胞电导对这些扰动的反应有相当大的变异性，并且在许多情况下注意到电流和电导之间有明显的解离。在稳态下，单个组织中细胞之间的变异性始终定义了氯化物细胞电流与电导之间的线性关系，零电流时电导截距为零。等效电路模型表明，单个组织内氯化物细胞的漏电导对单个氯化物细胞总电导的贡献比例始终相同，使得氯化物细胞的主动和漏电途径的电导之比恒定。漏电途径几乎肯定由钠选择性细胞旁途径主导。结果表明这些细胞控制其细胞旁途径的通透性。讨论了这种控制的一种可能机制。
