Ferrier J, Ward-Kesthely A, Heersche J N, Aubin J E
Medical Research Council Group in Periodontal Physiology, Faculty of Dentistry, University of Toronto, Ontario, Canada.
Bone Miner. 1988 Jun;4(2):133-45.
A multiphasic alteration in membrane potential occurs in response to calcitonin (CT), parathyroid hormone (PTH) and dibutyryl cAMP in the osteoblast-like UMR 106.01 and UMR 106.06 cell lines. This response consists of a small transient hyperpolarization, followed by a transient depolarization, followed by a long-term hyperpolarization. Experiments with channel blockers indicate that the depolarizing phase results from deactivation of K+ channels that are blocked by quinine but not by tetraethylammonium (TEA), and that the long-term hyperpolarization results from activation of K+ channels that are not blocked by quinine or by TEA. Correlating with the stimulation of intracellular cAMP by CT, a small percentage of the UMR 106.06 cells, but not UMR 106.01 cells, contract in response to CT. Both cell lines show a larger percentage of cells contracting in response to PTH than to CT.
在成骨样UMR 106.01和UMR 106.06细胞系中，降钙素（CT）、甲状旁腺激素（PTH）和二丁酰环磷腺苷（dibutyryl cAMP）会引发膜电位的多相变化。这种反应包括一个小的短暂超极化，接着是短暂去极化，随后是长期超极化。使用通道阻滞剂进行的实验表明，去极化阶段是由被奎宁阻断但不被四乙铵（TEA）阻断的钾通道失活引起的，而长期超极化是由不被奎宁或TEA阻断的钾通道激活引起的。与CT对细胞内cAMP的刺激相关，一小部分UMR 106.06细胞（而非UMR 106.01细胞）会对CT产生收缩反应。两种细胞系中，对PTH产生收缩反应的细胞百分比均高于对CT产生收缩反应的细胞百分比。
