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无髓鞘轴突中传导延迟历史依赖性的离子机制。

Ionic mechanisms underlying history-dependence of conduction delay in an unmyelinated axon.

作者信息

Zhang Yang, Bucher Dirk, Nadim Farzan

机构信息

Department of Mathematical Sciences, New Jersey Institute of Technology, Newark, United States.

Federated Department of Biological Sciences, NJIT and Rutgers University, Newark, United States.

出版信息

Elife. 2017 Jul 10;6:e25382. doi: 10.7554/eLife.25382.

Abstract

Axonal conduction velocity can change substantially during ongoing activity, thus modifying spike interval structures and, potentially, temporal coding. We used a biophysical model to unmask mechanisms underlying the history-dependence of conduction. The model replicates activity in the unmyelinated axon of the crustacean stomatogastric pyloric dilator neuron. At the timescale of a single burst, conduction delay has a non-monotonic relationship with instantaneous frequency, which depends on the gating rates of the fast voltage-gated Na current. At the slower timescale of minutes, the mean value and variability of conduction delay increase. These effects are because of hyperpolarization of the baseline membrane potential by the Na/K pump, balanced by an h-current, both of which affect the gating of the Na current. We explore the mechanisms of history-dependence of conduction delay in axons and develop an empirical equation that accurately predicts this history-dependence, both in the model and in experimental measurements.

摘要

轴突传导速度在持续活动期间会发生显著变化,从而改变动作电位间隔结构,并有可能改变时间编码。我们使用了一个生物物理模型来揭示传导的历史依赖性背后的机制。该模型复制了甲壳类动物口胃幽门扩张神经元无髓鞘轴突中的活动。在单个爆发的时间尺度上,传导延迟与瞬时频率呈非单调关系,这取决于快速电压门控钠电流的门控速率。在较慢的分钟时间尺度上,传导延迟的平均值和变异性会增加。这些效应是由于钠钾泵使基线膜电位超极化,并由h电流平衡,这两者都会影响钠电流的门控。我们探索了轴突中传导延迟的历史依赖性机制,并开发了一个经验方程,该方程能准确预测模型和实验测量中的这种历史依赖性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd24/5519330/3d3c356ba316/elife-25382-fig1.jpg

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