Calcium role in depolarization-secretion coupling: an aequorin study in squid giant synapse.
Calcium role in depolarization-secretion coupling: an aequorin study in squid giant synapse.
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钙在去极化-分泌耦合中的作用：鱿鱼巨突触中的水母发光蛋白研究。
DOI：
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发表时间：
1975
影响因子：
11.1
通讯作者：
C. Nicholson
中科院分区：
文献类型：
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作者：
R. Llinás;C. Nicholson
Aequorin是一种在有钙存在的情况下发光的蛋白质，它被注射到鱿鱼巨型突触的突触前末端。在注射之前，细胞内注射四乙基铵，这延长了突触前动作电位的持续时间。在这一过程之后，光发射是由能够释放突触递质的单个突触前棘波引起的。在第二组实验中，突触前注射四乙基铵后，细胞外注射河豚毒素，这会消除突触前动作电位。在这种情况下，突触前终末的人工去极化以一种分级的方式触发突触递质的释放。然而，正如其他作者以前报道的那样，膜电位阶跃到大约+90 mV(抑制电位)的内部正值会在施加电位的持续时间内阻止递质释放。然而，随着当前注射的终止，突触传递再次出现。在突触前纤维细胞内注射水飞蓟素后进行的一组类似的实验表明，水飞蓟素的光反应是由能够释放突触递质的膜电位步骤引起的。如果膜电位正向“抑制”水平，则在电流脉冲结束时，不会引起光响应，但会出现光发射和发射器释放。这些实验表明，递质的释放与细胞内钙离子浓度直接相关，抑制电位与突触前终末存在钙平衡电位是相容的。
Aequorin, a protein that emits light in the presence of calcium, was injected in the presynaptic terminal of the squid giant synapse. This injection was preceded by intracellular tetraethylammonium administration, which prolonged the duration of the presynaptic action potential. After this procedure light emission was evoked by single presynaptic spikes capable of releasing synaptic transmitter. In a second set of experiments, presynaptic tetraethylammonium injection was followed by the administration of tetrodotoxin extracellularly, which abolished the presynaptic action potential. Under these conditions artificial depolarization of the presynaptic terminal triggered the release of synaptic transmitter, in a graded manner. However, as previously reported by other authors, membrane potential steps to an internal positive value of approximately plus 90 mV (the suppression potential) produced a blockage of transmitter release for the duration of the imposed potential. Synaptic transmission recurred, nevertheless, as the current injection was terminated. A similar set of experiments, performed after the intracellular injection of aequorin in the presynaptic fiber, demonstrated that the aequorin light response was evoked by membrane potential steps capable of releasing synaptic transmitter. If the membrane potential was made positive to the "suppression" level, no light response was evoked but the light emission appeared, as did transmitter release, at the end of the current pulse. These experiments demonstrate that release of transmitter is directly correlated with intracellular calcium concentration and that the suppression potential is compatible with the existence of a calcium equilibrium potential at the presynaptic terminal.