Role of intracellular Ca2+ in stimulation-induced increases in transmitter release at the frog neuromuscular junction.
Role of intracellular Ca2+ in stimulation-induced increases in transmitter release at the frog neuromuscular junction.
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细胞内 Ca2 在刺激诱导的青蛙神经肌肉接头递质释放增加中的作用。
DOI：
10.1085/jgp.104.2.337
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Mosier,DR
中科院分区：
文献类型：
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作者：
Zengel,JE;Sosa,MA;Poage,RE;Mosier,DR
在量子含量减少的条件下，突触前神经的重复刺激可以导致该神经响应于刺激而释放的递质的量的逐渐增加。在青蛙神经肌肉接头处，这种释放的增加归因于四个不同的过程：易化、增强和增强的第一和第二组分（例如，Zengel，J.E.，和K. L.麦格尔比1982.普通生理学杂志。80：583-611）。有人认为，增加的Ca 2+的进入或内端Ca 2+的积累可能是负责一个或多个这些过程。为了验证这一假设，我们研究了细胞内Ca 2+介导的终板电位（EPP）振幅的变化过程中和重复刺激后在青蛙神经肌肉接头的作用。我们发现，增加细胞外Ca 2+浓度或暴露的准备，以羰基氰间氯苯腙，离子霉素，或cyclopiazonic酸都导致更大的增加EPP振幅在条件列车的10-200脉冲施加在频率为20脉冲/秒。这些实验操作，所有这些都已被证明增加细胞内的Ca 2+水平，似乎主要通过增加释放增加的增强成分起作用。这项研究的结果是一致的，与以前的建议，增加释放的不同组件代表不同的机制，和Ca 2+可能会在一个以上的网站在神经末梢。
Under conditions of reduced quantal content, repetitive stimulation of a presynaptic nerve can result in a progressive increase in the amount of transmitter released by that nerve in response to stimulation. At the frog neuromuscular junction, this increase in release has been attributed to four different processes: first and second components of facilitation, augmentation, and potentiation (e.g., Zengel, J. E., and K. L. Magleby. 1982. Journal of General Physiology. 80:583-611). It has been suggested that an increased entry of Ca2+ or an accumulation of intraterminal Ca2+ may be responsible for one or more of these processes. To test this hypothesis, we have examined the role of intracellular Ca2+ in mediating changes in end-plate potential (EPP) amplitude during and after repetitive stimulation at the frog neuromuscular junction. We found that increasing the extracellular Ca2+ concentration or exposing the preparation to carbonyl cyanide m-chlorophenylhydrazone, ionomycin, or cyclopiazonic acid all led to a greater increase in EPP amplitude during conditioning trains of 10-200 impulses applied at a frequency of 20 impulses/s. These experimental manipulations, all of which have been shown to increase intracellular levels of Ca2+, appeared to act by increasing primarily the augmentation component of increased release. The results of this study are consistent with previous suggestions that the different components of increased release represent different mechanisms, and that Ca2+ may be acting at more than one site in the nerve terminal.