Calcitonin (CT)-secreting cells (C-cells) are remarkably sensitive to changes in the extracellular Ca2+ concentration. In order to detect the mechanism by which C-cells monitor Ca2+, we compared a C-cell line responding to Ca2+ (rMTC cells) with another one known to have a defect in this Ca2+ signal transduction (TT cells). Rises of the Ca2+ concentration caused rMTC cells to depolarize and/or elicited spontaneous action potentials. Under voltage-clamp conditions, rMTC cells showed a slowly decaying Ca2+ inward current which was sensitive to dihydropyridines but not to Ni2+ at a low concentration. In contrast, the 'defective' TT cells neither depolarized nor fired action potentials with high Ca2+; they only exhibited an Ni2(+)-sensitive, transient Ca2+ current. The data strongly suggest that the slowly inactivating Ca2+ current is a prerequisite for Ca2(+)-sensitivity of C-cells and that fast inactivating channels are not sufficient to act as sensors of the extracellular Ca2+ concentration.

译文

:分泌降钙素(CT)的细胞(C细胞)对细胞外Ca2浓度的变化非常敏感。为了检测C细胞监测Ca2的机制,我们将响应Ca2的C细胞系(rMTC细胞)与已知在Ca2信号转导中存在缺陷的另一种细胞(TT细胞)进行了比较。 Ca 2浓度的升高引起rMTC细胞去极化和/或引起自发动作电位。在电压钳制条件下,rMTC细胞显示出缓慢衰减的Ca2内向电流,该电流对二氢吡啶敏感,但对低浓度的Ni2不敏感。相反,“缺陷”的TT细胞既没有去极化也没有激发具有高Ca2的动作电位。它们仅表现出对Ni2()敏感的瞬态Ca2电流。数据强烈表明,缓慢失活的Ca2电流是C细胞对Ca2()敏感性的先决条件,而快速失活的通道不足以充当细胞外Ca2浓度的传感器。

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