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本文引用的文献

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[Ultrastructural and cytochemical data on the mechanism of acetylcholine release in synaptic transmission]].[关于突触传递中乙酰胆碱释放机制的超微结构和细胞化学数据]
Arch Ital Biol. 1973 Dec;111(3-4):231-62.
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Disruption of syntaxin-mediated protein interactions blocks neurotransmitter secretion.Syntaxin介导的蛋白质相互作用的破坏会阻断神经递质的分泌。
Proc Natl Acad Sci U S A. 1997 Oct 28;94(22):12186-91. doi: 10.1073/pnas.94.22.12186.
3
Binding of the synaptic vesicle v-SNARE, synaptotagmin, to the plasma membrane t-SNARE, SNAP-25, can explain docked vesicles at neurotoxin-treated synapses.突触小泡的v-SNARE蛋白(突触结合蛋白)与质膜的t-SNARE蛋白(SNAP-25)的结合,可以解释在经神经毒素处理的突触处停靠的小泡。
Proc Natl Acad Sci U S A. 1997 Feb 4;94(3):997-1001. doi: 10.1073/pnas.94.3.997.
4
Synaptotagmin-syntaxin interaction: the C2 domain as a Ca2+-dependent electrostatic switch.突触结合蛋白- syntaxin相互作用:作为Ca2+依赖型静电开关的C2结构域
Neuron. 1997 Jan;18(1):133-42. doi: 10.1016/s0896-6273(01)80052-0.
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Bipartite Ca2+-binding motif in C2 domains of synaptotagmin and protein kinase C.突触结合蛋白和蛋白激酶C的C2结构域中的二分体钙离子结合基序
Science. 1996 Jul 12;273(5272):248-51. doi: 10.1126/science.273.5272.248.
6
A novel function for the second C2 domain of synaptotagmin. Ca2+-triggered dimerization.突触结合蛋白第二个C2结构域的新功能。钙离子触发的二聚化。
J Biol Chem. 1996 Mar 8;271(10):5844-9. doi: 10.1074/jbc.271.10.5844.
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Localization of synaptotagmin-binding domains on syntaxin.Syntaxin上突触结合蛋白结合结构域的定位
J Neurosci. 1996 Mar 15;16(6):1975-81. doi: 10.1523/JNEUROSCI.16-06-01975.1996.
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Calcium-induced translocation of synaptic vesicles to the active site.钙诱导突触小泡向活性位点的转运。
J Neurosci. 1993 Jun;13(6):2313-22. doi: 10.1523/JNEUROSCI.13-06-02313.1993.
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A role for synaptotagmin (p65) in regulated exocytosis.突触结合蛋白(p65)在调节性胞吐作用中的作用。
Cell. 1993 Jan 15;72(1):153-9. doi: 10.1016/0092-8674(93)90059-y.
10
Synaptic function is impaired but not eliminated in C. elegans mutants lacking synaptotagmin.在缺乏突触结合蛋白的秀丽隐杆线虫突变体中,突触功能受损但并未消除。
Cell. 1993 Jul 2;73(7):1291-305. doi: 10.1016/0092-8674(93)90357-v.

在果蝇的突触结合蛋白突变体中,形态学上对接的突触小泡数量减少。

Morphologically docked synaptic vesicles are reduced in synaptotagmin mutants of Drosophila.

作者信息

Reist N E, Buchanan J, Li J, DiAntonio A, Buxton E M, Schwarz T L

机构信息

Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523, USA.

出版信息

J Neurosci. 1998 Oct 1;18(19):7662-73. doi: 10.1523/JNEUROSCI.18-19-07662.1998.

DOI:10.1523/JNEUROSCI.18-19-07662.1998
PMID:9742137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6793008/
Abstract

Nerve terminal specializations include mechanisms for maintaining a subpopulation of vesicles in a docked, fusion-ready state. We have investigated the relationship between synaptotagmin and the number of morphologically docked vesicles by an electron microscopic analysis of Drosophila synaptotagmin (syt) mutants. The overall number of synaptic vesicles in a terminal was reduced, although each active zone continued to have a cluster of vesicles in its vicinity. In addition, there was an increase in the number of large vesicles near synapses. Examining the clusters, we found that the pool of synaptic vesicles immediately adjacent to the presynaptic membrane, the pool that includes the docked population, was reduced to 24 +/- 5% (means +/- SEM) of control in the sytnull mutation. To separate contributions of overall vesicle depletion and increased spontaneous release from direct effects of synaptotagmin on morphological docking, we examined syt mutants in an altered genetic background. Recombining syt alleles onto a second chromosome bearing an as yet uncharacterized mutation resulted in the expected decrease in evoked release but suppressed the increase in spontaneous release frequency. Motor nerve terminals in this genotype contained more synaptic vesicles than control, yet the number of vesicles immediately adjacent to the presynaptic membrane near active zones was still reduced (33 +/- 4% of control). Our findings demonstrate that there is a decrease in the number of morphologically docked vesicles seen in syt mutants. The decreases in docking and evoked release are independent of the increase in spontaneous release. These results support the hypothesis that synaptotagmin stabilizes the docked state.

摘要

神经末梢特化包括将一部分囊泡维持在停靠状态(即准备好融合的状态)的机制。我们通过对果蝇突触结合蛋白(syt)突变体进行电子显微镜分析,研究了突触结合蛋白与形态学上停靠的囊泡数量之间的关系。尽管每个活性区附近仍有一群囊泡,但终末中突触囊泡的总数减少了。此外,突触附近大囊泡的数量增加。检查这些囊泡群时,我们发现紧邻突触前膜的突触囊泡池(包括停靠囊泡群体的那个池)在syt基因敲除突变体中减少到对照的24±5%(平均值±标准误)。为了区分总体囊泡耗竭和自发释放增加的影响与突触结合蛋白对形态学停靠的直接作用,我们在改变的遗传背景下检查了syt突变体。将syt等位基因重组到带有一个尚未鉴定突变的第二条染色体上,导致诱发释放预期减少,但抑制了自发释放频率的增加。这种基因型的运动神经末梢含有比对照更多的突触囊泡,然而活性区附近紧邻突触前膜的囊泡数量仍然减少(为对照的33±4%)。我们的研究结果表明,在syt突变体中可见形态学上停靠的囊泡数量减少。停靠和诱发释放的减少与自发释放的增加无关。这些结果支持了突触结合蛋白稳定停靠状态这一假说。