Villarroel A, Marrion N V, Lopez H, Adams P R
Howard Hughes Medical Institute, Department of Neurobiology and Behavior, SUNY, Stony Brook 11794-5230.
FEBS Lett. 1989 Sep 11;255(1):42-6. doi: 10.1016/0014-5793(89)81057-9.
We studied the action of bradykinin (BK) on ionic currents in fused pheochromocytoma PC12 cells under voltage-clamp in whole-cell mode, and on intracellular calcium using fura-2 BK induced the development of an outward current associated with an increase in intracellular calcium, followed by inhibition of an M-like current. The outward current was blocked by (+)-tubocurarine, and prevented when the calcium BAPTA or high concentrations of inositol 1,4,5-triphosphate were introduced into the cell, whereas the M-like current and its inhibition by BK remained unaffected. The protein kinase activator phorbol 12,13 dibutyrate partially reduced the M-current. M-current density did not substantially change after prolonged treatment with nerve growth factor.
我们在全细胞模式下的电压钳制条件下,研究了缓激肽(BK)对融合嗜铬细胞瘤PC12细胞离子电流的作用,以及使用fura-2对细胞内钙的作用。BK诱导了与细胞内钙增加相关的外向电流的产生,随后抑制了M样电流。外向电流被(+)-筒箭毒碱阻断,当将钙缓冲剂BAPTA或高浓度的肌醇1,4,5-三磷酸引入细胞时,外向电流被阻止,而M样电流及其被BK的抑制作用不受影响。蛋白激酶激活剂佛波醇12,13-二丁酸酯部分降低了M电流。用神经生长因子长期处理后,M电流密度没有显著变化。