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本文引用的文献

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Optical quantal analysis of synaptic transmission in wild-type and rab3-mutant Drosophila motor axons.野生型和 rab3 突变果蝇运动轴突突触传递的光量子分析。
Nat Neurosci. 2011 Apr;14(4):519-26. doi: 10.1038/nn.2767. Epub 2011 Mar 6.
2
Active zones and the readily releasable pool of synaptic vesicles at the neuromuscular junction of the mouse.活跃区和突触小泡的易释放池在小鼠的神经肌肉接头处。
J Neurosci. 2011 Feb 9;31(6):2000-8. doi: 10.1523/JNEUROSCI.4663-10.2011.
3
A novel form of presynaptic plasticity based on the fast reactivation of release sites switched off during low-frequency depression.一种基于在低频抑制期间关闭的释放位点快速重新激活的新型突触前可塑性。
J Neurosci. 2010 Dec 8;30(49):16679-91. doi: 10.1523/JNEUROSCI.3644-09.2010.
4
Bassoon speeds vesicle reloading at a central excitatory synapse.巴松管加速中央兴奋性突触囊泡的再加载。
Neuron. 2010 Nov 18;68(4):710-23. doi: 10.1016/j.neuron.2010.10.026.
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Naked dense bodies provoke depression.裸致密体引起抑郁。
J Neurosci. 2010 Oct 27;30(43):14340-5. doi: 10.1523/JNEUROSCI.2495-10.2010.
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Mechanisms of short-term plasticity at neuromuscular active zones of Drosophila.果蝇神经肌肉活动区的短期可塑性机制。
HFSP J. 2010 Apr;4(2):72-84. doi: 10.2976/1.3338710. Epub 2010 Apr 8.
7
The active zone T-bar--a plasticity module?活性区T形杆——一个可塑性模块?
J Neurogenet. 2010 Sep;24(3):133-45. doi: 10.3109/01677063.2010.489626.
8
Unraveling mechanisms of homeostatic synaptic plasticity.解析平衡型突触可塑性的机制。
Neuron. 2010 May 13;66(3):337-51. doi: 10.1016/j.neuron.2010.04.028.
9
A hierarchy of cell intrinsic and target-derived homeostatic signaling.细胞内在和靶源性稳态信号的层次结构。
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10
Rapid structural alterations of the active zone lead to sustained changes in neurotransmitter release.快速的活性区结构改变导致神经递质释放的持续变化。
Proc Natl Acad Sci U S A. 2010 May 11;107(19):8836-41. doi: 10.1073/pnas.0906087107. Epub 2010 Apr 26.

在突触可塑性过程中快速活跃区重塑。

Rapid active zone remodeling during synaptic plasticity.

机构信息

Carl Ludwig Institute of Physiology, Medical Faculty, University of Leipzig, 04103 Leipzig, Germany.

出版信息

J Neurosci. 2011 Apr 20;31(16):6041-52. doi: 10.1523/JNEUROSCI.6698-10.2011.

DOI:10.1523/JNEUROSCI.6698-10.2011
PMID:21508229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6632979/
Abstract

How can synapses change the amount of neurotransmitter released during synaptic plasticity? Although release in general is intensely investigated, its determinants during plasticity are still poorly understood. As a model for plastic strengthening of synaptic release, we here use the well-established presynaptic homeostatic compensation during interference with postsynaptic glutamate receptors at the Drosophila neuromuscular junction. Combining short-term plasticity analysis, cumulative EPSC analysis, fluctuation analysis, and quantal short-term plasticity modeling, we found an increase in the number of release-ready vesicles during presynaptic strengthening. High-resolution light microscopy revealed an increase in the amount of the active zone protein Bruchpilot and an enlargement of the presynaptic cytomatrix structure. Furthermore, these functional and structural alterations of the active zone were not only observed after lifelong but already after minutes of presynaptic strengthening. Our results demonstrate that presynaptic plasticity can induce active zone remodeling, which regulates the number of release-ready vesicles within minutes.

摘要

在突触可塑性过程中,突触如何改变神经递质的释放量?尽管目前对释放过程进行了深入研究,但对其在可塑性过程中的决定因素仍知之甚少。作为突触释放可塑性增强的模型,我们在此使用在果蝇肌神经接点中干扰突触后谷氨酸受体后的已建立的突触前内在稳态补偿。通过结合短期可塑性分析、累积 EPSC 分析、波动分析和量子短期可塑性建模,我们发现突触前增强过程中,准备释放的囊泡数量增加。高分辨率的荧光显微镜显示,活性区蛋白 Bruchpilot 的含量增加,并且突触前细胞基质结构增大。此外,这些活性区的功能和结构改变不仅在终生观察到,而且在几分钟的突触前增强后即可观察到。我们的研究结果表明,突触前可塑性可以诱导活性区重塑,在几分钟内调节准备释放的囊泡数量。