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首页> 外文期刊>The European Journal of Neuroscience >The role of voltage dependence of the NMDA receptor in cellular and network oscillation
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The role of voltage dependence of the NMDA receptor in cellular and network oscillation

机译：NMDA受体的电压依赖性在细胞和网络振荡中的作用

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摘要

Unraveling the mechanisms underlying oscillatory behavior is critical for understanding normal and pathological brain processes. Here we used electrophysiology in mouse neocortical slices and principles of nonlinear dynamics to demonstrate how an increase in the N-methyl-d-aspartic acid receptor (NMDAR) conductance can create a nonlinear whole-cell current-voltage (I-V) relationship which leads to changes in cellular stability. We discovered two behaviorally and morphologically distinct pyramidal cell populations. Under control conditions, both cell types responded to depolarizing current injection with regular spiking patterns. However, upon NMDAR activation, an intrinsic oscillatory (IO) cell type (n=44) showed a nonlinear whole-cell I-V relationship, intrinsic voltage-dependent oscillations plus amplification of alternating input current, and these properties persisted after disabling action potential generation with tetrodotoxin (TTX). The other non-oscillatory (NO) neuronal population (n=24) demonstrated none of these behaviors. Simultaneous intra- and extracellular recordings demonstrated the NMDAR's capacity to promote low-frequency seizure-like network oscillations via its effects on intrinsic neuronal properties. The two pyramidal cell types demonstrated different relationships with network oscillation - the IO cells were leaders that were activated early in the population activity cycle while the activation of the NO cell type was distributed across network bursts. The properties of IO neurons disappeared in a low-magnesium environment where the voltage dependence of the receptor is abolished; concurrently, the cellular contribution to network oscillation switched to synchronous firing. Thus, depending upon the efficacy of NMDAR in altering the linearity of the whole-cell I-V relationship, the two cell populations played different roles in sustaining network oscillation. Unraveling the mechanisms underlying oscillatory behavior is critical for understanding normal and pathological brain processes. Here we used electrophysiology in mouse neocortical slices and principles of nonlinear dynamics to demonstrate how an increase in the N-methyl-d-aspartic acid receptor (NMDAR) conductance can create a nonlinear whole-cell current-voltage (I-V) relationship which leads to changes in cellular stability.
机译：弄清振荡行为的潜在机制对于理解正常和病理性大脑过程至关重要。在这里，我们使用小鼠新皮质切片中的电生理学和非线性动力学原理来证明N-甲基-d-天冬氨酸受体（NMDAR）电导的增加如何产生非线性全细胞电流-电压（IV）关系，从而导致细胞稳定性的变化。我们发现了两个行为和形态上截然不同的锥体细胞群。在控制条件下，两种电池类型均以规则的尖峰模式响应去极化电流注入。但是，在NMDAR激活后，固有振荡（IO）细胞类型（n = 44）显示出非线性的全细胞IV关系，固有电压依赖性振荡以及交流输入电流的放大，并且在禁用动作电位生成后这些特性仍然存在。河豚毒素（TTX）。其他非振荡（NO）神经元群体（n = 24）均未表现出这些行为。同时的细胞内和细胞外记录表明，NMDAR通过对内在神经元特性的影响而促进低频癫痫样网络振荡。两种金字塔形细胞类型显示出与网络振荡的不同关系-IO细胞是在种群活动周期的早期被激活的引导者，而NO细胞类型的激活则分布在整个网络突发中。在低镁环境中，IO神经元的特性消失了，在低镁环境中，受体的电压依赖性消失了。同时，蜂窝对网络振荡的贡献切换为同步触发。因此，取决于NMDAR改变全细胞I-V关系的线性的功效，两个细胞群在维持网络振荡中起着不同的作用。弄清振荡行为的潜在机制对于理解正常和病理性大脑过程至关重要。在这里，我们使用小鼠新皮质切片中的电生理学和非线性动力学原理来证明N-甲基-d-天冬氨酸受体（NMDAR）电导的增加如何产生非线性全细胞电流-电压（IV）关系，从而导致细胞稳定性的变化。

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