Asymmetry in signal propagation between the soma and dendrites plays a key role in determining dendritic excitability in motoneurons.
Asymmetry in signal propagation between the soma and dendrites plays a key role in determining dendritic excitability in motoneurons.
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DOI：
10.1371/journal.pone.0095454
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Heckman CJ
中科院分区：
文献类型：
--
作者：
Kim H;Jones KE;Heckman CJ
人们普遍认为，电生理信号在神经元胞体和树突之间的传播因方向不同而不同，即不对称。这种不对称性如何影响电压门控树突状通道的激活，以及随后的神经元行为，目前尚不清楚。基于对几种运动神经元不对称性的分析，我们扩展了我们以前的方法，将完全重建的运动神经元模型简化为保持信号传播不对称的两室表示。简化的模型准确地复制了树突的兴奋性和解剖学模型中涉及分散在树突上的持续内向电流(PIC)的动力学。用简化的模型研究了不对称信号传播与树枝的兴奋性之间的关系，同时用PIC密度常数改变了胞体和树枝之间信号传播的不对称性。我们发现，从胞体到树突的信号衰减增加增加了PIC(低兴奋性)的激活阈值，而从树突到胞体的信号衰减增加降低了PIC(高兴奋性)的激活阈值。这些效应是如此强烈，以至于逆转了胞体-树突-树突-胞体衰减的不对称性，逆转了PIC阈值与该电流源到胞体的距离之间的相关性。我们提出了不对称信号传播与枝晶中输入电阻的紧密关系作为不对称信号传播影响枝晶激发性的机制。所有这些结果强调了维持树突状细胞信号的生理不对称性的重要性，不仅对于细胞的正常功能，而且对于树突状细胞兴奋性的生物物理模拟。
It is widely recognized that propagation of electrophysiological signals between the soma and dendrites of neurons differs depending on direction, i.e. it is asymmetric. How this asymmetry influences the activation of voltage-gated dendritic channels, and consequent neuronal behavior, remains unclear. Based on the analysis of asymmetry in several types of motoneurons, we extended our previous methodology for reducing a fully reconstructed motoneuron model to a two-compartment representation that preserved asymmetric signal propagation. The reduced models accurately replicated the dendritic excitability and the dynamics of the anatomical model involving a persistent inward current (PIC) dispersed over the dendrites. The relationship between asymmetric signal propagation and dendritic excitability was investigated using the reduced models while varying the asymmetry in signal propagation between the soma and the dendrite with PIC density constant. We found that increases in signal attenuation from soma to dendrites increased the activation threshold of a PIC (hypo-excitability), whereas increases in signal attenuation from dendrites to soma decreased the activation threshold of a PIC (hyper-excitability). These effects were so strong that reversing the asymmetry in the soma-to-dendrite vs. dendrite-to-soma attenuation, reversed the correlation between PIC threshold and distance of this current source from the soma. We propose the tight relation of the asymmetric signal propagation to the input resistance in the dendrites as a mechanism underlying the influence of the asymmetric signal propagation on the dendritic excitability. All these results emphasize the importance of maintaining the physiological asymmetry in dendritic signaling not only for normal function of the cells but also for biophysically realistic simulations of dendritic excitability.
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