Cahalan M D, Hall J
J Gen Physiol. 1982 Mar;79(3):411-36. doi: 10.1085/jgp.79.3.411.
Alamethicin, a peptide antibiotic, partitions into artificial lipid bilayer membranes and into frog myelinated nerve membranes, inducing a voltage-dependent conductance. Discrete changes in conductance representing single-channel events with multiple open states can be detected in either frog node or lipid bilayer membranes. In 120 mM salt solution, the average conductance of a single channel is approximately 600 pS. The channel lifetimes are roughly two times longer in the node membrane than in a phosphatidylethanolamine bilayer at the same membrane potential. With 2 or 20 mM external Ca and internal CsCl, the alamethicin-induced conductance of frog nodal membrane inactivates. Inactivation is abolished by internal EGTA, suggesting that internal accumulation of calcium ions is responsible for the inactivation, through binding of Ca to negative internal surface charges. As a probe for both external and internal surface charges, alamethicin indicates a surface potential difference of approximately -20 to -30 mV, with the inner surface more negative. This surface charge asymmetry is opposite to the surface potential distribution near sodium channels.
短杆菌肽A是一种肽抗生素,可分配到人工脂质双分子层膜和青蛙有髓神经膜中,诱导电压依赖性电导。在青蛙节点或脂质双分子层膜中均可检测到代表具有多个开放状态的单通道事件的电导离散变化。在120 mM盐溶液中,单个通道的平均电导约为600 pS。在相同膜电位下,通道在节点膜中的寿命大约是在磷脂酰乙醇胺双分子层中的两倍。在外部Ca为2或20 mM且内部为CsCl的情况下,短杆菌肽A诱导的青蛙节点膜电导失活。内部EGTA可消除失活,这表明钙离子的内部积累是通过Ca与内部负表面电荷结合而导致失活的原因。作为外部和内部表面电荷的探针,短杆菌肽A表明表面电位差约为-20至-30 mV,内表面更负。这种表面电荷不对称与钠通道附近的表面电位分布相反。