Arnaudeau S, Leprêtre N, Mironneau J
Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, Centre National de la Recherche Scientifique, Unite de Recherche Associée 1489, Université de Bordeaux II, France.
Am J Obstet Gynecol. 1994 Aug;171(2):491-501. doi: 10.1016/0002-9378(94)90288-7.
The purpose of our study was to characterize the membrane mechanisms responsible for oxytocin-induced depolarization in single cells from pregnant rat myometrium.
Membrane currents were recorded with the whole-cell mode of the standard patch-clamp technique. Intracellular calcium concentration was monitored with the fluorescence from Fura 2 added to the pipette solution.
We found that oxytocin predominantly activates potassium, chloride, and cation conductances. Chloride and cation currents were evoked by an increase in the intracellular calcium concentration dependent on calcium release from the heparin-sensitive intracellular stores. Chloride and cation current showed different calcium dependences so that they could be activated separately.
Stimulation of oxytocin receptors induces opening of calcium-activated chloride and cation channels, leading to depolarization of the myometrial cells. This depolarization opens, in turn, voltage-dependent calcium channels.
我们研究的目的是描述负责催产素诱导的妊娠大鼠子宫肌层单细胞去极化的膜机制。
采用标准膜片钳技术的全细胞模式记录膜电流。用添加到移液管溶液中的Fura 2荧光监测细胞内钙浓度。
我们发现催产素主要激活钾、氯和阳离子电导。氯和阳离子电流由细胞内钙浓度的增加引起，这取决于从肝素敏感的细胞内储存中释放钙。氯和阳离子电流表现出不同的钙依赖性，因此它们可以被分别激活。
催产素受体的刺激诱导钙激活的氯和阳离子通道开放，导致子宫肌层细胞去极化。反过来，这种去极化打开电压依赖性钙通道。
