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单个海马突触处单量子幅度的双脉冲抑制

Paired-pulse depression of unitary quantal amplitude at single hippocampal synapses.

作者信息

Chen Gong, Harata Nobutoshi C, Tsien Richard W

机构信息

Department of Molecular and Cellular Physiology, Beckman Center, Stanford University School of Medicine, Stanford, CA 94305, USA.

出版信息

Proc Natl Acad Sci U S A. 2004 Jan 27;101(4):1063-8. doi: 10.1073/pnas.0307149101. Epub 2004 Jan 13.

DOI:10.1073/pnas.0307149101
PMID:14722357
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC327151/
Abstract

At central synapses, quantal size is generally regarded as fluctuating around a fixed mean with little change during short-term synaptic plasticity. We evoked quantal release by brief electric stimulation at single synapses visualized with FM 1-43 dye in hippocampal cultures. The majority of quantal events evoked at single synapses were monovesicular, based on examination of amplitude distribution of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-mediated responses. Consistent with previous findings, the quantal size did not change during paired-pulse facilitation (PPF), supporting the notion that the evoked events were monoquantal. However, during paired-pulse depression (PPD), there was a significant decrease in unitary quantal size, which was not due to postsynaptic receptor desensitization. This asymmetry of quantal modulation during PPF and PPD was demonstrated at the same single synapse at different extracellular calcium concentrations. Our results indicate that PPF can be fully accounted for by an increase of release probability, whereas PPD may be caused by decreases in both release probability and quantal size. One possible explanation is that the release of a quantum of neurotransmitter from synaptic vesicles is not invariant but subject to rapid calcium-dependent modulation during short-term synaptic plasticity.

摘要

在中枢突触中,量子大小通常被认为围绕一个固定均值波动,在短期突触可塑性期间变化很小。我们通过在海马体培养物中用FM 1-43染料可视化的单个突触处进行短暂电刺激来诱发量子释放。基于对α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体介导反应的幅度分布检查,在单个突触处诱发的大多数量子事件是单囊泡的。与先前的发现一致,在双脉冲易化(PPF)期间量子大小没有变化,支持了诱发事件是单量子的观点。然而,在双脉冲抑制(PPD)期间,单位量子大小显著减小,这不是由于突触后受体脱敏。在不同细胞外钙浓度下,在同一个单突触处证明了PPF和PPD期间量子调制的这种不对称性。我们的结果表明,PPF可以完全由释放概率的增加来解释,而PPD可能是由释放概率和量子大小的降低引起的。一种可能的解释是,从突触小泡释放的神经递质量子不是不变的,而是在短期突触可塑性期间受到快速钙依赖性调制。

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