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首页> 外文期刊>Journal of Computational Neuroscience >Influences of membrane properties on phase response curve and synchronization stability in a model globus pallidus neuron
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Influences of membrane properties on phase response curve and synchronization stability in a model globus pallidus neuron

机译：膜性质对苍白球神经元模型的相响应曲线和同步稳定性的影响

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The activity patterns of the globus pallidus (GPe) and subthalamic nucleus (STN) are closely associated with motor function and dysfunction in the basal ganglia. In the pathological state caused by dopamine depletion, the STN— GPe network exhibits rhythmic synchronous activity accompanied by rebound bursts in the STN. Therefore, the mechanism of activity transition is a key to understand basal ganglia functions. As synchronization in GPe neurons could induce pathological STN rebound bursts, it is important to study how synchrony is generated in the GPe. To clarify this issue, we applied the phase-reduction technique to a conductance-based GPe neuronal model in order to derive the phase response curve (PRC) and interaction function between coupled GPe neurons. Using the PRC and interaction function, we studied how the steady-state activity of the GPe network depends on intrinsic membrane properties, varying ionic conductances on the membrane. We noted that a change in persistent sodium current, fast delayed rectifier Kv3 potassium current, M-type potassium current and small conductance calcium-dependent potassium current influenced the PRC shape and the steady state. The effect of those currents on the PRC shape could be attributed to extension of the firing period and reduction of the phase response immediately after an action potential. In particular, the slow potassium current arising from the M-type potassium and the SK current was responsible for the reduction of the phase response. These results suggest that the membrane property modulation controls synchronization/asynchronization in the GPe and the pathological pattern of STN-GPe activity.
机译：苍白球（GPe）和丘脑下核（STN）的活动模式与基底神经节的运动功能和功能障碍密切相关。在由多巴胺耗竭引起的病理状态下，STN-GPe网络表现出节律性同步活动，并伴有STN中的反弹爆发。因此，活动过渡机制是了解基底神经节功能的关键。由于GPe神经元中的同步可诱导病理性STN反弹爆发，因此研究GPe中如何产生同步非常重要。为了弄清这个问题，我们将相减技术应用于基于电导的GPe神经元模型，以得出耦合GPe神经元之间的相位响应曲线（PRC）和相互作用函数。使用PRC和相互作用函数，我们研究了GPe网络的稳态活动如何取决于固有的膜特性，膜上不同的离子电导率。我们注意到持续钠电流，快速延迟整流Kv3钾电流，M型钾电流和小电导钙依赖性钾电流的变化影响了PRC形状和稳态。这些电流对PRC形状的影响可以归因于在动作电位之后立即延长了点火时间和减小了相位响应。特别是，由M型钾和SK电流引起的钾电流缓慢是造成相响应降低的原因。这些结果表明，膜性质调节控制GPe中的同步/非同步以及STN-GPe活性的病理模式。

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