Calcium‐induced inactivation of calcium current causes the inter‐burst hyperpolarization of Aplysia bursting neurones.
Calcium‐induced inactivation of calcium current causes the inter‐burst hyperpolarization of Aplysia bursting neurones.
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钙诱导的钙电流失活导致海兔爆发神经元的爆发间超极化。
DOI：
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发表时间：
1985
期刊：
影响因子：
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通讯作者：
R. Zucker
中科院分区：
文献类型：
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作者：
R. Kramer;R. Zucker
在先前的论文中描述了在动脉瘤神经元L2-L 6中跟随去极化电压钳脉冲的一系列三相尾电流（克雷默和Zucker，1985）。在本文中，我们研究了尾电流（III相）的晚期外向成分的性质，该成分在未夹紧的细胞中产生爆发间超极化。III相尾电流在-30 mV和-90 mV之间不会反向，并且对外部K+浓度相对不敏感。相反，细胞内Ca 2+注射引起的Ca 2+依赖性K+电流（IK（Ca））在-65 mV附近逆转，逆转电位对外部K+浓度敏感。向浸浴介质中加入50 mM-四乙基铵（TEA）会导致III相尾电流小幅增加。相反，IK（Ca）通过添加50 mM-TEA完全阻断。III相尾电流被接近ECa的去极化脉冲抑制，被Ca 2+电流拮抗剂（Co 2+和Mn 2+）阻断，并且被EGTA的细胞内注射阻断。在完全去除细胞外Na+后，III相尾电流减少不到10%。这些爆发神经元具有电压依赖性Ca 2+电导，其在与未夹紧细胞的平均静息电位（即-40 mV）相似的膜电位下表现出稳态激活。稳态Ca 2+电导可以通过Ca 2+注入或通过产生大量Ca 2+流入的去极化预脉冲而失活。稳态Ca 2+电导具有与III相尾电流相似的电压依赖性。稳态Ca 2+电导的Ca 2+依赖性失活与III相尾电流平行发生;两者对Ca 2+内流具有相似的敏感性，并且在去极化脉冲后两个过程以相似的速率衰减。因此，我们提出III相尾电流是由于稳态Ca 2+电导的Ca 2+依赖性失活。与III相尾电流和爆发间超极化（数十秒）的时间过程相比，模拟尖峰或尖峰爆发后IK（Ca）的衰减较快（小于1 s）。因此，我们得出结论，IK（Ca）在这些细胞中终止爆发或产生爆发间超极化中没有主要作用。我们提出了一个定性模型的离子基础的爆裂起搏器周期。该模型的中心特征是Ca 2+电流的电压依赖性激活和Ca 2+依赖性失活。
A triphasic series of tail currents which follow depolarizing voltage‐clamp pulses in Aplysia neurones L2‐L6 was described in the preceding paper (Kramer & Zucker, 1985). In this paper, we examine the nature of the late outward component of the tail current (phase III) which generates the inter‐burst hyperpolarization in unclamped cells. The phase III tail current does not reverse between ‐30 and ‐90 mV, and is relatively insensitive to the external K+ concentration. In contrast, Ca2+‐dependent K+ current (IK(Ca)), elicited by intracellular Ca2+ injection, reverses near ‐65 mV, and the reversal potential is sensitive to the external K+ concentration. Addition of 50 mM‐tetraethylammonium (TEA) to the bathing medium causes a small increase in the phase III tail current. In contrast, IK(Ca) is completely blocked by addition of 50 mM‐TEA. The phase III tail current is suppressed by depolarizing pulses which approach ECa, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA. The phase III tail current is reduced by less than 10% after complete removal of extracellular Na+. These bursting neurones have a voltage‐dependent Ca2+ conductance which exhibits steady‐state activation at a membrane potential similar to the average resting potential of the unclamped cell (i.e. ‐40 mV). The steady‐state Ca2+ conductance can be inactivated by Ca2+ injection, or by depolarizing pre‐pulses which generate a large influx of Ca2+. The steady‐state Ca2+ conductance has a voltage dependence similar to that of the phase III tail current. The Ca2+‐dependent inactivation of the steady‐state Ca2+ conductance occurs in parallel with the phase III tail current; both have a similar sensitivity to Ca2+ influx, and both processes decay with similar rates after a depolarizing pulse. Hence, we propose that the phase III tail current is due to the Ca2+‐ dependent inactivation of a steady‐state Ca2+ conductance. The decay of IK(Ca) following simulated spikes or bursts of spikes is rapid (less than 1 s) compared to the time course of the phase III tail current and the inter‐burst hyperpolarization (tens of seconds). Thus, we conclude that IK(Ca) does not have a major role in terminating bursts or generating the inter‐burst hyperpolarization in these cells. We present a qualitative model of the ionic basis of the bursting pace‐maker cycle. The central features of the model are the voltage‐dependent activation and the Ca2+‐dependent inactivation of a Ca2+ current.
海兔 L2-L6 神经元细胞内钾离子活性和膜电位响应常氧和缺氧的可逆变化。
DOI：
10.1242/jeb.102.1.79
发表时间：
1983
期刊：
The Journal of experimental biology
影响因子：
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作者：
Coyer,PE;HalseyJr,JH;Strong,ER
通讯作者：
Strong,ER