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首页> 外文期刊>PLoS Computational Biology >Spike-Timing Dependence of Structural Plasticity Explains Cooperative Synapse Formation in the Neocortex
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Spike-Timing Dependence of Structural Plasticity Explains Cooperative Synapse Formation in the Neocortex

机译:结构可塑性的穗时间依赖性解释了新皮层中协同突触的形成。

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摘要

Structural plasticity governs the long-term development of synaptic connections in the neocortex. While the underlying processes at the synapses are not fully understood, there is strong evidence that a process of random, independent formation and pruning of excitatory synapses can be ruled out. Instead, there must be some cooperation between the synaptic contacts connecting a single pre- and postsynaptic neuron pair. So far, the mechanism of cooperation is not known. Here we demonstrate that local correlation detection at the postsynaptic dendritic spine suffices to explain the synaptic cooperation effect, without assuming any hypothetical direct interaction pathway between the synaptic contacts. Candidate biomolecular mechanisms for dendritic correlation detection have been identified previously, as well as for structural plasticity based thereon. By analyzing and fitting of a simple model, we show that spike-timing correlation dependent structural plasticity, without additional mechanisms of cross-synapse interaction, can reproduce the experimentally observed distributions of numbers of synaptic contacts between pairs of neurons in the neocortex. Furthermore, the model yields a first explanation for the existence of both transient and persistent dendritic spines and allows to make predictions for future experiments.
机译:结构可塑性支配着新皮层中突触连接的长期发展。虽然对突触的基本过程尚未完全了解,但有力的证据表明,可以排除随机,独立形成和修剪兴奋性突触的过程。相反,在连接单个突触前和突触后神经元对的突触接触之间必须有某种合作。到目前为止,合作机制尚不清楚。在这里,我们证明了在突触后树突棘上进行局部相关性检测就足以解释突触的协同作用,而无需假设任何假设的突触接触之间的直接相互作用途径。先前已经确定了用于树突相关检测的候选生物分子机制,以及基于其的结构可塑性。通过分析和拟合一个简单的模型,我们表明,与时序关联相关的结构可塑性,没有交叉突触相互作用的其他机制,可以重现实验性观察到的新皮层中神经元对之间的突触接触数量分布。此外,该模型对瞬时树突棘和持久树突棘的存在都给出了第一个解释,并为未来的实验做出了预测。

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