REGULATION OF TRANSMITTER RELEASE AT THE SQUID GIANT SYNAPSE BY PRESYNAPTIC DELAYED RECTIFIER POTASSIUM CURRENT
REGULATION OF TRANSMITTER RELEASE AT THE SQUID GIANT SYNAPSE BY PRESYNAPTIC DELAYED RECTIFIER POTASSIUM CURRENT
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DOI：
10.1113/jphysiol.1990.sp018333
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发表时间：
1990-12-01
影响因子：
5.5
通讯作者：
AUGUSTINE, GJ
中科院分区：
文献类型：
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作者：
AUGUSTINE, GJ
1.应用三微电极电压钳技术和药物对鱿鱼巨突触前末梢钾电流的性质和功能进行了研究。2.外向电流由两个组成部分：一个缓慢的组件，激活超过数百毫秒，并被阻断的细胞外应用的四乙基铵（TEA）离子和更迅速的激活组件，这是相对不敏感的细胞外TEA。3.通过用细胞外TEA以及河豚毒素（阻断钠通道电流）和锰（阻断钙通道电流）处理突触前末梢，在隔离中研究了更快速的组分。该电流分量的幅度在0 mV时为1-2 mA cm-2。激活和失活的速率是电压依赖性的，并且对于持续时间小于几秒的去极化，几乎没有失活的证据。4.在生理盐水中，电流的逆转电位为-70至-80 mV，并且随着细胞外钾浓度的升高而变得更正，表明钾是主要的渗透离子。细胞外钾的积累似乎是显着的去极化过程中产生显着的激活电流。5. 3，4-二氨基吡啶（DAP）的细胞外应用阻断了电流，在0 mV下表观解离常数为7 μ M。细胞内应用DAP和TEA也有效地降低了该电流。这些治疗，但不是细胞外TEA的应用，扩大了突触前动作电位，并增加了幅度和时间的突触后电流引起的扩大突触前动作电位的峰值。突触后电流是动作电位时程的敏感和线性函数;动作电位时程增加30%，突触后电流幅度增加190%。6.突触前钙电流的幅度和时间过程的估计，根据以前的测量钙通道门控，表明动作电位增宽产生的钙电流幅度大幅增加。这些计算预测，再突触动作电位时程增加30%将使钙电流的峰值幅度增加约230%。这意味着在动作电位期间递质释放和钙进入之间存在线性关系，并且可以通过假设钙协同触发不重叠的细胞内结构域内的释放来解释。7.这些结果表明，“延迟整流”钾通道是鱿鱼突触前末梢的主要钾通道，这些通道通过调节动作电位持续时间，从而调节突触前钙离子进入量，在递质释放中发挥关键作用。负责慢外向电流的通道似乎在决定动作电位波形中没有作用。
1. The three-microelectrode voltage clamp technique and pharmacological agents were used to examine the properties and functions of potassium currents in squid giant presynaptic terminals. 2. Outward currents consisted of two components: a slow component which acitvated over hundreds of milliseconds and was blocked by extracellular application of tetraethylammonium (TEA) ions and a more rapidly activating component which was relatively insensitive to extracellular TEA. 3. The more rapid component was studied in isolation by treating prsynapitc terminals with extracellular TEA , as well as tetrodotoxin (to block sodium channel currents) and manganese (to block calcium channel currents). The magnitude of this current component was 1-2 mA cm-2 at 0 mV. Rate of activation and deactivation were voltage dependent and little evidence of inactivation was seen for depolarizatino less than several seconds in duration. 4. The reversal potential of the current was -70 to -80 mV in normal saline and became more positive with elevated extracellular potassium concentrations, suggesting that potassium is the primary permeant ion. Accumulation of extracellular potassium appeared to be marked during depolarizations that produced significant activation of the current. 5. Extracellular application of 3,4-diaminopyridine (DAP) blocked the current with an apparent dissociation constant of 7 .mu.M at 0 mV. Intracellular applications of DAP and TEA also were effective in reducing this current. These treatments, but not extracellular TEA application, broadened presynaptic action potentials and increased the magnitude and time-to-peak of postsynaptic currents elicited by the broadened presynaptic action potentials. Postsynaptic currents were a sensitive and linear function of action potential duration; a 30% increase in action potential duration increased postsynaptic current amplitude by 190%. 6. Estimation of the magnitude and time course of the presynaptic calcium curent, based on previous measurements of calcium channel gating, indicated that action potential broadening produces a large increase in calcium current magnitude. These calculations predict that a 30% increase in resynaptic action potential duration will increase the peak amplitude of the calcium current by approximately 230%. This implies a linear relationship between transmitter release and calcium entry during an action potential and can be explained by assuming that calcium co-operatively triggers release within intracellular domains that do not overlap. 7. These results indicate that ''delayed rectifier'' potassium channels are the predominant potassium channels of squid presynaptic terminals and that these channels play a critical role in transmitter release by regulating action potentil duration and, thereby, the amount of presynatpic calcium entry. The channels responisble for the slow outward current appear to have no role in determining action potential waveform.