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首页> 外文期刊>Journal of Neurophysiology >Membrane channel interactions underlying rat subthalamic projection neuron rhythmic and bursting activity.
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Membrane channel interactions underlying rat subthalamic projection neuron rhythmic and bursting activity.

机译：大鼠丘脑底投射神经元的节律和爆发活动的膜通道相互作用。

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A computational model of the rat subthalamic nucleus projection neuron is constructed using electrophysiological and morphological data and a restricted set of channel specifications. The model cell exhibits a wide range of electrophysiological behaviors characteristic of rat subthalamic neurons. It reveals that a key set of three channels play a primary role in distinguishing behaviors: a high-voltage-activated calcium channel (Cav 1.2.-1.3), a low-voltage-activated calcium channel (Cav 3.-), and a small current calcium-activated potassium channel (KCa 2.1-2.3). Short and long posthyperpolarization rebound responses, low-frequency rhythmic bursting (< 1 Hz), higher-frequency rhythmic bursting (4-7 Hz), and slow action and depolarizing potentials are behaviors all mediated by the interaction of these channels. This interaction can generate a robust calcium-dependent extended depolarization in the dendrites (a depolarizing plateau). The diversity observed in the rat subthalamic physiology (such as shortor long rebounds, or the presence of low-frequency rhythmic busting) can arise from alterations in both the density and distributions of these channel types and, consequently, their ability to generate this depolarizing plateau. A number of important predictions arise from the model. For example, blocking or disrupting the low-voltage-activated Cav 3.- calcium current should mute the emergence of rebound responses and rhythmic bursting. Conversely, increasing this channel current via large hyperpolarizing potentials in combination with partial blockade of the high-voltage-activated calcium channels should lead to the more experimentally elusive in vitro high-frequency bursting.
机译：使用电生理和形态学数据以及一组受限的通道规范来构建大鼠丘脑丘脑底核投射神经元的计算模型。模型细胞表现出大鼠丘脑下神经元广泛的电生理行为特征。它揭示了一组关键的三个通道在区分行为中起主要作用：高压激活钙通道（Cav 1.2.-1.3），低压激活钙通道（Cav 3.-）和小电流钙激活钾通道（KCa 2.1-2.3）。超极化后的短期和长期反弹反应，低频节律性猝发（<1 Hz），高频节律性猝发（4-7 Hz）以及动作缓慢和去极化电位都是由这些通道的相互作用介导的行为。这种相互作用可以在树突中产生强大的钙依赖性扩展去极化作用（去极化平稳期）。在大鼠丘脑底生理中观察到的多样性（例如较短或较长的反弹，或低频节律性破坏的存在）可能是由于这些通道类型的密度和分布的变化，以及它们产生这种去极化平台的能力的变化引起的。该模型产生了许多重要的预测。例如，阻断或破坏低压激活的Cav 3-钙电流应使反弹反应和节律性爆发的出现静音。相反，通过较大的超极化电势结合部分阻断高压激活的钙离子通道来增加该通道电流，应导致体外高频猝发实验上更加难以捉摸。

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