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本文引用的文献

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Astrocyte signaling controls spike timing-dependent depression at neocortical synapses.星形胶质细胞信号控制新皮层突触的依赖于发放频率的突触抑制。
Nat Neurosci. 2012 Mar 25;15(5):746-53. doi: 10.1038/nn.3075.
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Pull-push neuromodulation of LTP and LTD enables bidirectional experience-induced synaptic scaling in visual cortex.牵拉-推动神经调节 LTP 和 LTD 实现了视觉皮层中双向经验诱导的突触可塑性。
Neuron. 2012 Feb 9;73(3):497-510. doi: 10.1016/j.neuron.2011.11.023.
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Molecular determinants controlling NMDA receptor synaptic incorporation.控制 NMDA 受体突触整合的分子决定因素。
J Neurosci. 2011 Apr 27;31(17):6311-6. doi: 10.1523/JNEUROSCI.5553-10.2011.
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Dendritic synapse location and neocortical spike-timing-dependent plasticity.树突状突触位置与新皮层尖峰时间依赖可塑性。
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Temporal modulation of spike-timing-dependent plasticity.时变调制的尖峰时间依赖可塑性。
Front Synaptic Neurosci. 2010 Jun 17;2:19. doi: 10.3389/fnsyn.2010.00019. eCollection 2010.
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In vivo spike-timing-dependent plasticity in the optic tectum of Xenopus laevis.活体非洲爪蟾顶盖的脉冲时间依赖性可塑性。
Front Synaptic Neurosci. 2010 Jun 10;2:7. doi: 10.3389/fnsyn.2010.00007. eCollection 2010.
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Spike timing dependent plasticity: a consequence of more fundamental learning rules.尖峰时间依赖可塑性:更基本学习规则的结果。
Front Comput Neurosci. 2010 Jul 1;4. doi: 10.3389/fncom.2010.00019. eCollection 2010.
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Metaplasticity at single glutamatergic synapses.单个谷氨酸能突触的转换可塑性。
Neuron. 2010 Jun 24;66(6):859-70. doi: 10.1016/j.neuron.2010.05.015.
9
A specific requirement of Arc/Arg3.1 for visual experience-induced homeostatic synaptic plasticity in mouse primary visual cortex.Arc/Arg3.1 对小鼠初级视觉皮层视觉经验诱导的同型突触可塑性的特定要求。
J Neurosci. 2010 May 26;30(21):7168-78. doi: 10.1523/JNEUROSCI.1067-10.2010.
10
Co-regulation of ocular dominance plasticity and NMDA receptor subunit expression in glutamic acid decarboxylase-65 knock-out mice.谷氨酸脱羧酶-65基因敲除小鼠中眼优势可塑性与NMDA受体亚基表达的共同调控
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暗适应延长了依赖于时间的峰电位可塑性的整合窗口。

Dark exposure extends the integration window for spike-timing-dependent plasticity.

机构信息

The Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, USA.

出版信息

J Neurosci. 2012 Oct 24;32(43):15027-35. doi: 10.1523/JNEUROSCI.2545-12.2012.

DOI:10.1523/JNEUROSCI.2545-12.2012
PMID:23100424
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3496177/
Abstract

Metaplasticity, the adaptive changes of long-term potentiation (LTP) and long-term depression (LTD) in response to fluctuations in neural activity is well documented in visual cortex, where dark rearing shifts the frequency threshold for the induction of LTP and LTD. Here we studied metaplasticity affecting spike-timing-dependent plasticity, in which the polarity of plasticity is determined not by the stimulation frequency, but by the temporal relationship between near-coincidental presynaptic and postsynaptic firing. We found that in mouse visual cortex the same regime of deprivation that restricts the frequency range for inducing rate-dependent LTD extends the integration window for inducing timing-dependent LTD, enabling LTD induction with random presynaptic and postsynaptic firing. Notably, the underlying mechanism for the changes in both rate-dependent and time-dependent LTD appears to be an increase of NR2b-containing NMDAR at the synapse. Thus, the rules of metaplasticity might manifest in opposite directions, depending on the plasticity-induction paradigms.

摘要

在视觉皮层中,已经有充分的证据表明,长时程增强(LTP)和长时程抑制(LTD)的适应性变化(即形塑)会对神经活动的波动做出反应,在这个区域中,暗适应会改变诱导 LTP 和 LTD 的频率阈值。在这里,我们研究了影响尖峰时间依赖型可塑性(STDP)的形塑,其中可塑性的极性不是由刺激频率决定,而是由近同时的突触前和突触后放电之间的时间关系决定。我们发现,在小鼠的视觉皮层中,同样的剥夺状态限制了诱导依赖于速率的 LTD 的频率范围,同时也扩展了诱导依赖于时间的 LTD 的整合窗口,从而使得随机的突触前和突触后放电也能够诱导 LTD。值得注意的是,对于依赖于速率和时间的 LTD 的变化,其潜在机制似乎是突触处含有 NR2b 的 NMDA 受体的增加。因此,形塑的规则可能会根据可塑性诱导的范例表现出相反的方向。