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尖峰时间依赖性可塑性:大鼠CA1锥体神经元树突整合的学习规则。

Spike timing-dependent plasticity: a learning rule for dendritic integration in rat CA1 pyramidal neurons.

作者信息

Campanac Emilie, Debanne Dominique

机构信息

INSERM U641, Faculté de médecine secteur nord, IFR 11, Marseille, F-13916, France.

出版信息

J Physiol. 2008 Feb 1;586(3):779-93. doi: 10.1113/jphysiol.2007.147017. Epub 2007 Nov 29.

Abstract

Long-term plasticity of dendritic integration is induced in parallel with long-term potentiation (LTP) or depression (LTD) based on presynaptic activity patterns. It is, however, not clear whether synaptic plasticity induced by temporal pairing of pre- and postsynaptic activity is also associated with synergistic modification in dendritic integration. We show here that the spike timing-dependent plasticity (STDP) rule accounts for long-term changes in dendritic integration in CA1 pyramidal neurons in vitro. Positively correlated pre- and postsynaptic activity (delay: +5/+50 ms) induced LTP and facilitated dendritic integration. Negatively correlated activity (delay: -5/-50 ms) induced LTD and depressed dendritic integration. These changes were not observed following positive or negative pairing with long delays (> +/-50 ms) or when NMDA receptors were blocked. The amplitude-slope relation of the EPSP was facilitated after LTP and depressed after LTD. These effects could be mimicked by voltage-gated channel blockers, suggesting that the induced changes in EPSP waveform involve the regulation of voltage-gated channel activity. Importantly, amplitude-slope changes induced by STDP were found to be input specific, indicating that the underlying changes in excitability are restricted to a limited portion of the dendrites. We conclude that STDP is a common learning rule for long-term plasticity of both synaptic transmission and dendritic integration, thus constituting a form of functional redundancy that insures significant changes in the neuronal output when synaptic plasticity is induced.

摘要

基于突触前活动模式,树突整合的长期可塑性与长时程增强(LTP)或长时程抑制(LTD)同时被诱导。然而,尚不清楚由突触前和突触后活动的时间配对所诱导的突触可塑性是否也与树突整合中的协同修饰相关。我们在此表明,尖峰时间依赖性可塑性(STDP)规则解释了体外培养的CA1锥体神经元中树突整合的长期变化。正相关的突触前和突触后活动(延迟:+5/+50毫秒)诱导LTP并促进树突整合。负相关活动(延迟:-5/-50毫秒)诱导LTD并抑制树突整合。在与长延迟(> +/-50毫秒)进行正或负配对后或当NMDA受体被阻断时,未观察到这些变化。LTP后EPSP的幅度-斜率关系得到促进,LTD后则受到抑制。这些效应可被电压门控通道阻滞剂模拟,表明EPSP波形的诱导变化涉及电压门控通道活性的调节。重要的是,发现由STDP诱导的幅度-斜率变化是输入特异性的,这表明兴奋性的潜在变化局限于树突的有限部分。我们得出结论,STDP是突触传递和树突整合长期可塑性的共同学习规则,从而构成一种功能冗余形式,确保在诱导突触可塑性时神经元输出发生显著变化。

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