Wachman Elliot S, Poage Robert E, Stiles Joel R, Farkas Daniel L, Meriney Stephen D
Center for Light Microscope Imaging and Biotechnology, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213, USA.
J Neurosci. 2004 Mar 24;24(12):2877-85. doi: 10.1523/JNEUROSCI.1660-03.2004.
The nature of presynaptic calcium (Ca(2+)) signals that initiate neurotransmitter release makes these signals difficult to study, in part because of the small size of specialized active zones within most nerve terminals. Using the frog motor nerve terminal, which contains especially large active zones, we show that increases in intracellular Ca(2+) concentration within 1 msec of action potential invasion are attributable to Ca(2+) entry through N-type Ca(2+) channels and are not uniformly distributed throughout active zone regions. Furthermore, changes in the location and magnitude of Ca(2+) signals recorded before and after experimental manipulations (omega-conotoxin GVIA, diaminopyridine, and lowered extracellular Ca(2+)) support the hypothesis that there is a remarkably low probability of a single Ca(2+) channel opening within an active zone after an action potential. The trial-to-trial variability observed in the spatial distribution of presynaptic Ca(2+) entry also supports this conclusion, which differs from the conclusions of previous work in other synapses.
引发神经递质释放的突触前钙(Ca(2+))信号的性质使得这些信号难以研究,部分原因是大多数神经末梢内的特化活性区尺寸较小。利用具有特别大的活性区的青蛙运动神经末梢,我们发现动作电位侵入后1毫秒内细胞内Ca(2+)浓度的增加归因于Ca(2+)通过N型Ca(2+)通道的内流,并且在整个活性区区域内分布并不均匀。此外,实验操作(ω-芋螺毒素GVIA、二氨基吡啶和降低细胞外Ca(2+))前后记录的Ca(2+)信号的位置和幅度变化支持了这样一种假说,即动作电位后活性区内单个Ca(2+)通道开放的概率非常低。在突触前Ca(2+)内流的空间分布中观察到的每次试验间的变异性也支持这一结论,这与之前在其他突触中的研究结论不同。