Lishko V K, Saĭchenko E A, Storchak L G, Gimmerl'reĭkh N G
Biokhimiia. 1990 Sep;55(9):1578-83.
The dependence of Ca2+ transport in synaptosomes along the channels formed by alpha-latrotoxin on [Ca2+]in and the feasibility of transport along these channels of other bivalent cations were studied. It was found that the concentration dependence of Ca2+ influx is nonlinear and is described by the Michaelis-Menten kinetics (Km = 1.07 +/- 0.19 mM). Mg2+, Ba2+, Sr2+, Mn2+ and Co2+ competitively inhibited the Ca2+ influx via latrotoxin channels. Studies with the use of the fluorescent Ca2+ probes, Quin-2 and Fura-2, revealed that these cations can also penetrate inside synaptosomes via latrotoxin channels. The bivalent cation influx via latrotoxin channels caused a decrease of the membrane potential of synaptosomes. The similarity of properties of latrotoxin and endogenous Ca2+ channels is discussed.
研究了突触体中Ca2+沿α-黑寡妇毒素形成的通道的转运对胞内[Ca2+]的依赖性,以及其他二价阳离子沿这些通道转运的可行性。发现Ca2+内流的浓度依赖性是非线性的,可用米氏动力学描述(Km = 1.07 +/- 0.19 mM)。Mg2+、Ba2+、Sr2+、Mn2+和Co2+竞争性抑制通过黑寡妇毒素通道的Ca2+内流。使用荧光Ca2+探针Quin-2和Fura-2的研究表明,这些阳离子也可通过黑寡妇毒素通道进入突触体内部。通过黑寡妇毒素通道的二价阳离子内流导致突触体膜电位降低。文中讨论了黑寡妇毒素与内源性Ca2+通道性质的相似性。