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突触小泡启动蛋白Munc13-1在大鼠视网膜的紧张性活性带状突触中不存在。

The synaptic vesicle priming protein Munc13-1 is absent from tonically active ribbon synapses of the rat retina.

作者信息

Schmitz F, Augustin I, Brose N

机构信息

Leibniz-Institute for Neurobiology, Department of Neurochemistry and Molecular Biology, Brenneckestrasse 6, 39118 Magdeburg, Germany.

出版信息

Brain Res. 2001 Mar 23;895(1-2):258-63. doi: 10.1016/s0006-8993(01)02078-9.

DOI:10.1016/s0006-8993(01)02078-9
PMID:11259787
Abstract

Ribbon synapses, for example of the retina, are specialized synapses that differ from conventional, phasically active synapses in several aspects. Ribbon synapses can tonically and yet very rapidly release neurotransmitter via synaptic vesicle exocytosis. This requires an optimization of the synaptic machinery and is at least partly due to the presence of synaptic ribbons that bind large numbers of synaptic vesicles and which are believed to participate in priming synaptic vesicles for exocytosis. In this paper we analyzed whether ribbon synapses of the retina employ similar priming factors, i.e. Munc13-1, as do conventional, non-ribbon containing phasically active synapses. We found that though present in conventional synapses of the retina Munc13-1 was completely absent from ribbon-containing synapses of the retina, both in the outer as well as in the inner plexiform layer. This indicates that ribbon synapses of the retina employ other, possibly more potent priming factors than phasically active conventional synapses.

摘要

例如视网膜中的带状突触,是一种特殊的突触,在几个方面不同于传统的、具有相位活性的突触。带状突触可以通过突触小泡胞吐作用持续且非常快速地释放神经递质。这需要对突触机制进行优化,并且至少部分归因于存在结合大量突触小泡的突触带,据信这些突触带参与使突触小泡为胞吐作用做好准备。在本文中,我们分析了视网膜的带状突触是否像传统的、不含突触带的具有相位活性的突触那样利用相似的引发因子,即Munc13-1。我们发现,虽然Munc13-1存在于视网膜的传统突触中,但在视网膜的含突触带的突触中却完全不存在,无论是在外网状层还是在内网状层。这表明视网膜的带状突触利用的是其他引发因子,可能比具有相位活性的传统突触的引发因子更强效。

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