Instituto Teófilo Hernando, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.
Biochem Biophys Res Commun. 2011 Jul 1;410(2):307-11. doi: 10.1016/j.bbrc.2011.05.138. Epub 2011 May 31.
Ca(2+) entry through the L-subtype (α(1D), Ca(v)1,3) of voltage-dependent calcium channels (VDCCs) seems to selectively regulate the endocytotic response after the application of a single depolarizing pulse to voltage-clamped bovine chromaffin cells. Here we have found that L channel blockade with nifedipine transformed the exocytotic responses elicited by a double-pulse protocol, from depression to facilitation. This apparent paradoxical effect was mimicked by pharmacological interventions that directly block endocytosis namely, dynasore, calmidazolium, GTP-γS and GDP-βS. This reinforces our view that Ca(2+) entry through PQ channels (α(1A); Ca(v)2.1) regulates fast exocytosis while Ca(2+) entry through L channels preferentially controls rapid endocytosis.
钙(2+)通过电压依赖性钙通道(VDCCs)的 L 亚型(α(1D),CaV1.3)进入似乎选择性地调节了在对电压钳制的牛肾上腺嗜铬细胞施加单个去极化脉冲后内吞作用的反应。在这里,我们发现,用硝苯地平阻断 L 通道将双脉冲方案引发的胞吐反应从抑制转变为易化。这种明显的矛盾效应被直接阻断内吞作用的药理学干预模拟,即 dynasore、calmidazolium、GTP-γS 和 GDP-βS。这进一步证实了我们的观点,即通过 PQ 通道(α(1A);CaV2.1)的 Ca(2+)进入调节快速胞吐作用,而通过 L 通道的 Ca(2+)进入优先控制快速内吞作用。