Zucker R S, Delaney K R, Mulkey R, Tank D W
Department of Molecular and Cell Biology, University of California, Berkeley 94720.
Ann N Y Acad Sci. 1991;635:191-207. doi: 10.1111/j.1749-6632.1991.tb36492.x.
This review gives some indication of the progress that has been made in understanding synaptic transmission by use of new methods for measuring and controlling presynaptic [Ca2+]i. Many unsolved problems remain. We still do not have a clear idea of the exact relationship between [Ca2+]i and transmitter release and whether this relationship is the same under all circumstances. The apparently different [Ca2+]i-dependence of evoked transmitter release and of PTP suggest multiple molecular sites of calcium action that remain to be identified. A complete and comprehensive model of transmitter release has yet to be devised, and questions raised by our experiments may indicate that it is still too early to try to construct a precise model. We also do not know just how serotonin acts to modulate transmitter release, only that it does not appear to alter either resting or entering calcium. Some of these questions may be approachable with the techniques described here; others are not and require different methods for their resolution. The work continues.
本综述展示了在利用测量和控制突触前[Ca2+]i的新方法来理解突触传递方面所取得的一些进展。许多未解决的问题依然存在。我们仍不清楚[Ca2+]i与递质释放的确切关系,以及这种关系在所有情况下是否相同。诱发递质释放和强直后增强(PTP)对[Ca2+]i的依赖性明显不同,这表明钙作用的多个分子位点仍有待确定。完整而全面的递质释放模型尚未设计出来,我们实验提出的问题可能表明现在尝试构建精确模型还为时过早。我们也不清楚血清素如何调节递质释放,只知道它似乎不会改变静息钙或进入的钙。这些问题中的一些可能可以用这里描述的技术来解决;其他问题则不行,需要不同的方法来解决。研究仍在继续。