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静息电位对突触易化动力学的影响。

Effect of holding potential on the dynamics of homosynaptic facilitation.

机构信息

Fishberg Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.

出版信息

J Neurosci. 2011 Jul 27;31(30):11039-43. doi: 10.1523/JNEUROSCI.2361-11.2011.

DOI:10.1523/JNEUROSCI.2361-11.2011
PMID:21795552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3152988/
Abstract

We study a form of short-term synaptic plasticity that was originally described as a graded potentiating effect of holding potential on spike-mediated synaptic transmission (Shimahara and Tauc, 1975). This form of plasticity has recently generated considerable interest, as it has become apparent that it is present in the mammalian brain (Clark and Häusser, 2006; Marder, 2006). It has been suggested that it adds a previously unappreciated analog component to spike-mediated synaptic transmission (Alle and Geiger, 2006, 2008). A limitation of most previous research in this area is that effects of holding potential have been studied in relative isolation. Presynaptic neurons are stimulated at low frequencies so that a second form of plasticity (homosynaptic facilitation) is not induced. Under physiological conditions, however, both forms of plasticity are likely to be coinduced. In this report, we study the two types of plasticity together in an experimentally advantageous preparation (the mollusk Aplysia californica). Somewhat surprisingly, we find that effects of holding potential can be relatively modest when presynaptic neurons are activated at low frequencies. Interestingly, however, changes in membrane potential are highly effective when homosynaptic facilitation is induced. In this situation, PSPs facilitate at an increased rate. To summarize, our research suggests a novel view of the effect of holding potential on synaptic transmission. We propose that, under physiological conditions, it modifies the dynamics of homosynaptic facilitation.

摘要

我们研究了一种短期突触可塑性形式,该形式最初被描述为保持电位对尖峰介导的突触传递的分级增强效应(Shimahara 和 Tauc,1975)。这种形式的可塑性最近引起了相当大的兴趣,因为显然它存在于哺乳动物大脑中(Clark 和 Häusser,2006;Marder,2006)。有人认为,它为尖峰介导的突触传递增加了以前未被重视的模拟成分(Alle 和 Geiger,2006,2008)。该领域以前的大多数研究的一个局限性是,保持电位的影响是在相对孤立的情况下进行研究的。在低频刺激突触前神经元,因此不会诱导第二种可塑性形式(同源易化)。然而,在生理条件下,这两种形式的可塑性很可能同时被诱导。在本报告中,我们在一种具有实验优势的制剂(加利福尼亚海兔 Aplysia californica)中一起研究了这两种类型的可塑性。令人有些惊讶的是,我们发现当突触前神经元在低频下被激活时,保持电位的影响可以相对较小。有趣的是,然而,当诱导同源易化时,膜电位的变化非常有效。在这种情况下,PSP 以增加的速率易化。总之,我们的研究提出了一种关于保持电位对突触传递影响的新观点。我们提出,在生理条件下,它改变了同源易化的动力学。

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本文引用的文献

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