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Essential functions of synapsins Ⅰ and Ⅱ in synaptic vesicle regulation

机译：突触素Ⅰ和Ⅱ在突触小泡调节中的基本功能

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Synaptic vesicles are coated by synapsins, phosphoproteins that account for 9% of the vesicle protein. To analyse the functions of these proteins, we have studied knockout mice lacking either synapsin Ⅰ, synapsin Ⅱ, or both. Mice lacking synapsins are viable and fertile with no gross anatomical abnormalities, but experience seizures with a frequency proportional to the number of mutant alleles. Synapsin-Ⅱ and double knockouts, but not synapsin-Ⅰ knockouts, exhibit decreased post-tetanic potentiation and severe synaptic depression upon repetitive stimulation. Intrinsic synaptic-vesicle membrane proteins, but not peripheral membrane proteins or other synaptic proteins, are slightly decreased in individual knockouts and more severely reduced in double knockouts, as is the number of synaptic vesicles. Thus synapsins are not required for neurite outgrowth, synaptogenesis or the basic mechanics of synaptic vesicle traffic, but are essential for accelerating this traffic during repetitive stimulation. The phenotype of the synapsin knockouts could be explained either by deficient recruitment of synaptic vesicles to the active zone, or by impaired maturation of vesicles at the active zone, both of which could lead to a secondary destabilization of synaptic vesicles.
机译：突触小泡被突触蛋白包被，磷蛋白占小泡蛋白的9％。为了分析这些蛋白质的功能，我们研究了缺失突触素Ⅰ和/或突触素Ⅱ的小鼠。缺乏突触素的小鼠是活的和可育的，没有明显的解剖学异常，但是其发作的频率与突变等位基因的数量成正比。 Synapsin-Ⅱ和双重敲除，但不是synapsin-Ⅰ敲除，在重复刺激后表现出降低的强直性后增强和严重的突触抑制。内在突触小泡膜蛋白，但不是外周膜蛋白或其他突触蛋白，在单个敲除中略有减少，而在双敲除中更严重地减少，如突触小泡的数目一样。因此，突触素不是神经突生长，突触发生或突触小泡运输的基本机制所必需的，但是对于在重复刺激期间加速这种运输是必不可少的。突触蛋白敲除的表型可以通过突触小泡向活性区的募集不足或在活性区的小泡成熟受损来解释，两者均可导致突触小泡的继发不稳定。

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