Calcium time course as a signal for spike-timing-dependent plasticity.
Calcium time course as a signal for spike-timing-dependent plasticity.
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DOI：
10.1152/jn.00803.2004
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发表时间：
2005-05
影响因子：
2.5
通讯作者：
J. Rubin;R. C. Gerkin;Guoqiang Bi;Carson C. Chow
中科院分区：
文献类型：
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作者：
J. Rubin;R. C. Gerkin;Guoqiang Bi;Carson C. Chow
钙离子被认为是突触尖峰时间依赖性可塑性（STDP）的突触后信号。我们研究这一假设与计算建模的基础上，从海马文化的实验结果，其中一些是在这里，其中对和三联体的突触前和突触后尖峰诱导增强和抑郁症在时间上不对称的方式。具体而言，我们提出了一套模型生化检测器，基于合理的分子途径，直接利用钙信号的时间过程来重现这些实验STDP结果。我们的模型具有模块化的结构，其中长时程增强（LTP）和抑郁症（LTD）的组件竞争，以确定最终的可塑性结果，这种竞争的一个方面是否决权，通过适当的钙时间过程抑制LTD。我们的模型的模拟也被证明是一致的，与经典的LTP和LTD引起的几个突触前刺激范例。总的来说，我们的研究结果提供了计算证据表明，虽然突触后钙的时间过程中包含足够的信息来区分各种实验的长期可塑性范例，小的变化的反向传播的动作电位或突触动力学的属性可以改变钙的时间过程的方式，将显着影响STDP诱导的任何检测器完全基于突触后钙。这可能解释了海马培养物中观察到的STDP结果的变异性，在重复应用单个实验方案下，以及在不同系统的多个尖峰实验中观察到的。
Calcium has been proposed as a postsynaptic signal underlying synaptic spike-timing-dependent plasticity (STDP). We examine this hypothesis with computational modeling based on experimental results from hippocampal cultures, some of which are presented here, in which pairs and triplets of pre- and postsynaptic spikes induce potentiation and depression in a temporally asymmetric way. Specifically, we present a set of model biochemical detectors, based on plausible molecular pathways, which make direct use of the time course of the calcium signal to reproduce these experimental STDP results. Our model features a modular structure, in which long-term potentiation (LTP) and depression (LTD) components compete to determine final plasticity outcomes; one aspect of this competition is a veto through which appropriate calcium time courses suppress LTD. Simulations of our model are also shown to be consistent with classical LTP and LTD induced by several presynaptic stimulation paradigms. Overall, our results provide computational evidence that, while the postsynaptic calcium time course contains sufficient information to distinguish various experimental long-term plasticity paradigms, small changes in the properties of back-propagation of action potentials or in synaptic dynamics can alter the calcium time course in ways that will significantly affect STDP induction by any detector based exclusively on postsynaptic calcium. This may account for the variability of STDP outcomes seen within hippocampal cultures, under repeated application of a single experimental protocol, as well as for that seen in multiple spike experiments across different systems.