Study of mechanism for synaptic vesicle recycling

在2005年4月1日和2008年3月31日期间，我们揭示了关于突触小泡(SV)回收的四个主要发现。1)。果蝇幼虫神经末梢的SVS有两条截然不同的内吞途径，两种内吞作用协同作用使突触的高频传递得以维持较长时间。2)。突触前神经末梢的活动区和非活动区存在两种类型的内吞作用。通过两种类型的Cmaina2+通道，启动了两条钙离子内流途径。由straightJacket基因编码的Ca~(2+)通道被认为是控制活动区内吞作用的通道。3)。目前还没有关于神经末梢存在Tuburin的报道。我们培育出了表达GF-微管蛋白的转基因果蝇。GFP-微管蛋白对神经刺激的反应改变了它们在神经末梢的分布。微管蛋白的增效剂紫杉醇改变了SVS在神经末梢的内吞和交通的程度。4)。在个体FLE高活动后，突触传递分两步增强。在早期，量子尺寸增大，随后量子含量增加。

We have revealed four main findings on synaptic vesicle (SV) recycling in the period of April first, 2005 and March 31st, 2008. 1). There are two distinct pathways for endocytosis of SVs at the nerve terminals of Drosophila larvae and synaptic transmission at high frequency is maintained for a long time by two types of endocytosis which work coordinately. 2). Two types of endocytosis occurs at the active-zone and non-active zone at presynaptic nerve terminals. Two pathways are initiated by Ca2+ influx through two types of Cmaina2+ channels. Ca2+ channels which are encoded by straightjacket gene are identified as the channels which control active-zone endocytosis. 3). There has been no report to show the existence of tuburin at the nerve terminals. We produced transgenic flies which expressed GF-tubulin. GFP-tubulin changed their distribution in nerve terminals in response to nerve stimulation. Taxol, a tabilizer of tubulin, changed extents of endocytosis and traffic of SVs in nerve terminals. 4). After high activity of individual flie, synaptic transmission was enhanced by two steps. In the early phase, the quantum size increased and then the quantal contents increased.