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本文引用的文献

1
Chemically induced long-term potentiation increases the number of perforated and complex postsynaptic densities but does not alter dendritic spine volume in CA1 of adult mouse hippocampal slices.化学诱导的长期增强作用增加了穿孔和复杂的突触后致密物的数量，但并未改变成年小鼠海马切片CA1区树突棘的体积。
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Presynaptic and postsynaptic roles of NO, cGK, and RhoA in long-lasting potentiation and aggregation of synaptic proteins.一氧化氮（NO）、环磷酸鸟苷依赖性蛋白激酶（cGK）和RhoA在突触蛋白的长时程增强和聚集过程中的突触前和突触后作用。
Neuron. 2005 Feb 3;45(3):389-403. doi: 10.1016/j.neuron.2005.01.011.
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Enhancement of synaptic plasticity through chronically reduced Ca2+ flux during uncorrelated activity.在不相关活动期间通过长期降低钙离子通量增强突触可塑性。
Neuron. 2004 Dec 2;44(5):835-49. doi: 10.1016/j.neuron.2004.11.013.
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alpha-Synuclein produces a long-lasting increase in neurotransmitter release.α-突触核蛋白使神经递质释放产生持久增加。
EMBO J. 2004 Nov 10;23(22):4506-16. doi: 10.1038/sj.emboj.7600451. Epub 2004 Oct 28.
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Structural basis of long-term potentiation in single dendritic spines.单个树突棘中长时程增强的结构基础。
Nature. 2004 Jun 17;429(6993):761-6. doi: 10.1038/nature02617. Epub 2004 Jun 9.
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Multiple, developmentally regulated expression mechanisms of long-term potentiation at CA1 synapses.CA1突触处长期增强的多种、受发育调控的表达机制。
J Neurosci. 2004 May 26;24(21):4903-11. doi: 10.1523/JNEUROSCI.0170-04.2004.
7
Optical quantal analysis indicates that long-term potentiation at single hippocampal mossy fiber synapses is expressed through increased release probability, recruitment of new release sites, and activation of silent synapses.光学量子分析表明，单个海马苔藓纤维突触处的长期增强作用是通过释放概率增加、新释放位点的募集以及沉默突触的激活来实现的。
J Neurosci. 2004 Apr 7;24(14):3618-26. doi: 10.1523/JNEUROSCI.3567-03.2004.
8
Presynaptic CaMKII is necessary for synaptic plasticity in cultured hippocampal neurons.突触前钙/钙调蛋白依赖性蛋白激酶II对培养的海马神经元的突触可塑性是必需的。
Neuron. 2004 Apr 8;42(1):129-41. doi: 10.1016/s0896-6273(04)00143-6.
9
Presynaptic induction of heterosynaptic associative plasticity in the mammalian brain.哺乳动物大脑中异突触联想可塑性的突触前诱导。
Nature. 2003 Dec 18;426(6968):841-5. doi: 10.1038/nature02194.
10
Optical quantal analysis reveals a presynaptic component of LTP at hippocampal Schaffer-associational synapses.光学量子分析揭示了海马体谢弗-联合突触处长时程增强的突触前成分。
Neuron. 2003 Jun 5;38(5):797-804. doi: 10.1016/s0896-6273(03)00325-8.

培养海马神经元可塑性过程中的早期突触前变化。

Early presynaptic changes during plasticity in cultured hippocampal neurons.

作者信息

Ninan Ipe, Liu Shumin, Rabinowitz Daniel, Arancio Ottavio

机构信息

Taub Institute and Department of Pathology, Columbia University, New York City, NY 10032, USA.

出版信息

EMBO J. 2006 Sep 20;25(18):4361-71. doi: 10.1038/sj.emboj.7601318. Epub 2006 Sep 7.

DOI:10.1038/sj.emboj.7601318
PMID:16957772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1570425/
Abstract

Long-lasting increase in synaptic strength is thought to underlie learning. An explosion of data has characterized changes in postsynaptic (pstS) AMPA receptor cycling during potentiation. However, changes occurring within the presynaptic (prS) terminal remain largely unknown. We show that appearance of new release sites during potentiation between cultured hippocampal neurons is due to (a) conversion of nonrecycling sites to recycling sites, (b) formation of new releasing sites from areas containing diffuse staining for the prS marker Vesicle-Associated Membrane Protein-2 and (c) budding of new recycling sites from previously existing recycling sites. In addition, potentiation is accompanied by a release probability increase in pre-existing boutons depending upon their individual probability. These prS changes precede and regulate fluorescence increase for pstS GFP-tagged-AMPA-receptor subunit GluR1. These results suggest that potentiation involves early changes in the prS terminal including remodeling and release probability increase of pre-existing synapses.

摘要

突触强度的长期增加被认为是学习的基础。大量数据描绘了突触后（pstS）AMPA受体在增强过程中的循环变化。然而，突触前（prS）终末内发生的变化在很大程度上仍然未知。我们发现，培养的海马神经元之间增强过程中新释放位点的出现是由于：（a）非循环位点转变为循环位点；（b）从含有prS标志物囊泡相关膜蛋白2弥散染色的区域形成新的释放位点；以及（c）从先前存在的循环位点出芽形成新的循环位点。此外，增强伴随着既有突触小体释放概率的增加，这取决于它们各自的概率。这些prS变化先于并调节pstS绿色荧光蛋白标记的AMPA受体亚基GluR1的荧光增加。这些结果表明，增强涉及prS终末的早期变化，包括既有突触的重塑和释放概率增加。