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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >IMPAIRMENT OF SYNAPTIC VESICLE CLUSTERING AND OF SYNAPTIC TRANSMISSION, AND INCREASED SEIZURE PROPENSITY, IN SYNAPSIN I-DEFICIENT MICE
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IMPAIRMENT OF SYNAPTIC VESICLE CLUSTERING AND OF SYNAPTIC TRANSMISSION, AND INCREASED SEIZURE PROPENSITY, IN SYNAPSIN I-DEFICIENT MICE

机译：突触糖蛋白I缺乏症小鼠的突触小囊簇和突触传递的损伤，以及易感性

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摘要

Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exofytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination, The organization of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area, This was in contrast to the organized;vesicle clusters present in terminals of wild-type animals, Release of glutamate from nerve endings, induced by K+, 4-aminopyridine, or a Ca2+ ionophore, was markedly decreased in synapsin I mutant mice, The recovery of synaptic transmission after depletion of neurotransmitter by high-frequency stimulation was greatly delayed, Finally, synapsin I-deficient mice exhibited a strikingly increased response to electrical stimulation, as measured by electrographic acid behavioral seizures, These results provide strong support for the hypothesis that synapsin I plays a key role in the regulation of nerve terminal function in mature synapses. [References: 21]
机译：已经提出，突触素I通过控制突触小泡对胞外突的可用性来参与神经递质释放的调节。为了进一步了解突触素I在成年神经末梢功能中的作用，我们研究了同源重组产生的突触素I缺陷小鼠，突触素I缺陷小鼠突触前末端突触小泡的组织发生了显着变化：密集的囊泡仅存在于活动区域的狭窄边缘，而大多数囊泡分散在整个末端区域，这与野生型动物的末端存在的有组织的囊泡簇，谷氨酸从神经末梢释放，在突触素I突变小鼠中K +，4-氨基吡啶或Ca2 +离子载体显着降低，通过高频刺激耗尽神经递质后，突触传递的恢复大大延迟，最后，突触素I缺陷小鼠表现出显着增加的反应电击酸行为癫痫发作对电刺激的影响，这些结果为关于突触素I在成熟突触中神经末梢功能的调节中起关键作用的假说。 [参考：21]

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