Koch Marta, Holt Matthew
Laboratory of Neurogenetics, VIB Center for the Biology of Disease and K.U. Leuven Center for Human Genetics, O&N4 Herestraat 49, 3000 Leuven, Belgium.
Biochim Biophys Acta. 2012 Aug;1821(8):1114-32. doi: 10.1016/j.bbalip.2012.02.008. Epub 2012 Feb 23.
Chemical synapses are specialist points of contact between two neurons, where information transfer takes place. Communication occurs through the release of neurotransmitter substances from small synaptic vesicles in the presynaptic terminal, which fuse with the presynaptic plasma membrane in response to neuronal stimulation. However, as neurons in the central nervous system typically only possess ~200 vesicles, high levels of release would quickly lead to a depletion in the number of vesicles, as well as leading to an increase in the area of the presynaptic plasma membrane (and possible misalignment with postsynaptic structures). Hence, synaptic vesicle fusion is tightly coupled to a local recycling of synaptic vesicles. For a long time, however, the exact molecular mechanisms coupling fusion and subsequent recycling remained unclear. Recent work now indicates a unique role for the plasma membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP(2)), acting together with the vesicular protein synaptotagmin, in coupling these two processes. In this work, we review the evidence for such a mechanism and discuss both the possible advantages and disadvantages for vesicle recycling (and hence signal transduction) in the nervous system. This article is part of a Special Issue entitled Lipids and Vesicular Transport.
化学突触是两个神经元之间的特殊接触点，信息传递在此发生。通信通过突触前终末中小的突触小泡释放神经递质物质来实现，这些小泡在神经元刺激下与突触前质膜融合。然而，由于中枢神经系统中的神经元通常仅拥有约200个小泡，高水平的释放会迅速导致小泡数量减少，同时还会导致突触前质膜面积增加（以及可能与突触后结构错位）。因此，突触小泡融合与突触小泡的局部再循环紧密相连。然而，长期以来，将融合与随后的再循环联系起来的确切分子机制仍不清楚。最近的研究表明，质膜脂质磷脂酰肌醇4,5 - 二磷酸（PIP(2)）与囊泡蛋白突触结合蛋白共同作用，在耦合这两个过程中发挥独特作用。在这项工作中，我们回顾了这种机制的证据，并讨论了神经系统中囊泡再循环（以及信号转导）可能的优缺点。本文是名为“脂质与囊泡运输”的特刊的一部分。
