Hall J E, Cahalan M D
J Gen Physiol. 1982 Mar;79(3):387-409. doi: 10.1085/jgp.79.3.387.
This paper discusses a calcium-dependent inactivation of alamethicin-induced conductance in asymmetric lipid bilayers. The bilayers used were formed with one leaflet of phosphatidyl ethanolamine (PE) and one of phosphatidyl serine (PS). Calcium, initially confined to the neutral lipid (PE) side, can pass through the open alamethicin channel to the negative lipid (PS) side, where it can bind to the negative lipid and reduce the surface potential. Under appropriate circumstances, the voltage-dependent alamethicin conductance is thereby inactivated. We have formulated a model for this process based on the diffusion of calcium in the aqueous phases and we show that the model describes the kinetic properties of the alamethicin conductance under various circumstances. EGTA on the PS side of the membrane reduces the effects of calcium dramatically as predicted by the model.
本文讨论了在不对称脂质双分子层中,钙依赖性对阿拉霉素诱导的电导的失活作用。所用的双分子层由一层磷脂酰乙醇胺(PE)和一层磷脂酰丝氨酸(PS)形成。钙最初局限于中性脂质(PE)一侧,可通过开放的阿拉霉素通道到达带负电荷的脂质(PS)一侧,在那里它可以与带负电荷的脂质结合并降低表面电位。在适当的情况下,电压依赖性的阿拉霉素电导由此失活。我们基于钙在水相中的扩散为此过程建立了一个模型,并且表明该模型描述了在各种情况下阿拉霉素电导的动力学特性。膜PS一侧的乙二醇双四乙酸(EGTA)如模型所预测的那样,显著降低了钙的作用。