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本文引用的文献

1
Selective shunting of the NMDA EPSP component by the slow afterhyperpolarization in rat CA1 pyramidal neurons.大鼠CA1锥体神经元中慢后超极化对NMDA兴奋性突触后电位成分的选择性分流
J Neurophysiol. 2007 May;97(5):3242-55. doi: 10.1152/jn.00422.2006. Epub 2007 Feb 28.
2
Spine Ca2+ signaling in spike-timing-dependent plasticity.在尖峰时间依赖性可塑性中的脊髓钙离子信号传导
J Neurosci. 2006 Oct 25;26(43):11001-13. doi: 10.1523/JNEUROSCI.1749-06.2006.
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Learning, aging and intrinsic neuronal plasticity.学习、衰老与神经元内在可塑性
Trends Neurosci. 2006 Oct;29(10):587-99. doi: 10.1016/j.tins.2006.08.005. Epub 2006 Aug 30.
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Spike timing-dependent plasticity: from synapse to perception.尖峰时间依赖性可塑性：从突触到感知。
Physiol Rev. 2006 Jul;86(3):1033-48. doi: 10.1152/physrev.00030.2005.
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Requirement of dendritic calcium spikes for induction of spike-timing-dependent synaptic plasticity.树突状钙峰对于诱导尖峰时间依赖性突触可塑性的需求。
J Physiol. 2006 Jul 1;574(Pt 1):283-90. doi: 10.1113/jphysiol.2006.111062. Epub 2006 May 4.
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Spatial segregation of neuronal calcium signals encodes different forms of LTP in rat hippocampus.大鼠海马体中神经元钙信号的空间隔离编码了不同形式的长时程增强。
J Physiol. 2006 Jan 1;570(Pt 1):97-111. doi: 10.1113/jphysiol.2005.098947. Epub 2005 Nov 10.
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Role of hippocampal Cav1.2 Ca2+ channels in NMDA receptor-independent synaptic plasticity and spatial memory.海马体Cav1.2钙离子通道在不依赖NMDA受体的突触可塑性和空间记忆中的作用。
J Neurosci. 2005 Oct 26;25(43):9883-92. doi: 10.1523/JNEUROSCI.1531-05.2005.
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Spike-timing-dependent synaptic plasticity depends on dendritic location.峰电位时间依赖型突触可塑性取决于树突位置。
Nature. 2005 Mar 10;434(7030):221-5. doi: 10.1038/nature03366.
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LTP and LTD: an embarrassment of riches.长时程增强和长时程抑制：丰富得令人为难。
Neuron. 2004 Sep 30;44(1):5-21. doi: 10.1016/j.neuron.2004.09.012.
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Heterosynaptic metaplastic regulation of synaptic efficacy in CA1 pyramidal neurons of rat hippocampus.大鼠海马体CA1锥体神经元中突触效能的异突触可塑性调节
Hippocampus. 2004;14(8):1011-25. doi: 10.1002/hipo.20021.

兴奋性突触后电位（EPSP）波形的变化调节了依赖于峰电位时间的可塑性的时间窗口。

Changes of the EPSP waveform regulate the temporal window for spike-timing-dependent plasticity.

作者信息

Fuenzalida Marco, Fernandez de Sevilla David, Buño Washington

机构信息

Instituto Cajal, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain.

出版信息

J Neurosci. 2007 Oct 31;27(44):11940-8. doi: 10.1523/JNEUROSCI.0900-07.2007.

DOI:10.1523/JNEUROSCI.0900-07.2007
PMID:17978034
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6673379/
Abstract

Using spike-timing-dependent plasticity (STDP) protocols that consist of pairing an EPSP and a postsynaptic backpropagating action potential (BAP), we investigated the contribution of the changes in EPSP waveform induced by the slow Ca2+-dependent K+-mediated afterhyperpolarization (sAHP) in the regulation of long-term potentiation (LTP). The "temporal window" between Schaffer collateral EPSPs and BAPs in CA1 pyramidal neurons required to induce LTP was narrowed by a reduction of the amplitude and decay time constant of the EPSP, which could be reversed with cyclothiazide. The EPSP changes were caused by the increased conductance induced by activation of the sAHP. Therefore, the EPSP waveform and its regulation by the sAHP are central in determining the duration of the temporal window for STDP, thus providing a possible dynamic regulatory mechanism for the encoding of cognitive processes.

摘要

我们使用由兴奋性突触后电位（EPSP）与突触后反向传播动作电位（BAP）配对组成的依赖于峰电位时间的可塑性（STDP）协议，研究了由缓慢的钙依赖性钾介导的超极化后电位（sAHP）诱导的EPSP波形变化在长时程增强（LTP）调节中的作用。诱导LTP所需的CA1锥体神经元中沙费尔侧支EPSP与BAP之间的“时间窗口”因EPSP幅度和衰减时间常数的降低而变窄，而环噻嗪可使其逆转。EPSP的变化是由sAHP激活诱导的电导增加引起的。因此，EPSP波形及其由sAHP的调节在确定STDP时间窗口的持续时间中起核心作用，从而为认知过程的编码提供了一种可能的动态调节机制。