Parnas H, Segel L, Dudel J, Parnas I
Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Dept of Neurobiology, Alexander Silberman Institute of Life Sciences, The Hebrew University, Jerusalem 91904, Israel.
Trends Neurosci. 2000 Feb;23(2):60-8. doi: 10.1016/s0166-2236(99)01498-8.
It has been suggested that depolarization per se can control neurotransmitter release, in addition to its role in promoting Ca2+ influx. The 'Ca2+ hypothesis' has provided an essential framework for understanding how Ca2+ entry and accumulation in nerve terminals controls transmitter release. Yet, increases in intracellular Ca2+ levels alone cannot account for the initiation and termination of release; some additional mechanism is needed. Several experiments from various laboratories indicate that membrane potential has a decisive role in controlling this release. For example, depolarization causes release when Ca2+ entry is blocked and intracellular Ca2+ levels are held at an elevated level. The key molecules that link membrane potential with release control have not yet been identified: likely candidates are presynaptic autoreceptors and perhaps the Ca2+ channel itself.
有人提出，除了在促进Ca2+内流方面的作用外，去极化本身也可以控制神经递质的释放。“Ca2+假说”为理解神经末梢中Ca2+的进入和积累如何控制递质释放提供了一个重要框架。然而，仅细胞内Ca2+水平的升高并不能解释释放的起始和终止；还需要一些其他机制。来自不同实验室的多项实验表明，膜电位在控制这种释放中起决定性作用。例如，当Ca2+进入被阻断且细胞内Ca2+水平维持在升高水平时，去极化会导致释放。将膜电位与释放控制联系起来的关键分子尚未确定：可能的候选者是突触前自身受体，也许还有Ca2+通道本身。
