Golomb David, Shedmi Anat, Curtu Rodica, Ermentrout G Bard
Department of Physiology, Faculty of Health Sciences, Ben-Gurion University, Be'er-Sheva, Israel.
J Neurophysiol. 2006 Feb;95(2):1049-67. doi: 10.1152/jn.00932.2005. Epub 2005 Oct 19.
We explore the mechanism of synchronized bursting activity with frequency of approximately 10 Hz that appears in cortical tissues at low extracellular magnesium concentration [Mg2+]o. We hypothesize that this activity is persistent, namely coexists with the quiescent state and depends on slow N-methyl-D-aspartate (NMDA) conductances. To explore this hypothesis, we construct and investigate a conductance-based model of excitatory cortical networks. Population bursting activity can persist for physiological values of the NMDA decay time constant (approximately 100 ms). Neurons are synchronized at the time scale of bursts but not of single spikes. A reduced model of a cell coupled to itself can encompass most of this highly synchronized network behavior and is analyzed using the fast-slow method. Synchronized bursts appear for intermediate values of the NMDA conductance g(NMDA) if NMDA conductances are not too fast. Regular spiking activity appears for larger g(NMDA). If the single cell is a conditional burster, persistent synchronized bursts become more robust. Weakly synchronized states appear for zero AMPA conductance g(AMPA). Enhancing g(AMPA) increases both synchrony and the number of spikes within bursts and decreases the bursting frequency. Too strong g(AMPA), however, prevents the activity because it enhances neuronal intrinsic adaptation. When [Mg2+]o is increased, higher g(NMDA) values are needed to maintain bursting activity. Bursting frequency decreases with [Mg2+]o, and the network is silent with physiological [Mg2+]o. Inhibition weakly decreases the bursting frequency if inhibitory cells receive enough NMDA-mediated excitation. This study explains the importance of conditional bursters in layer V in supporting epileptiform activity at low [Mg2+]o.
我们探究了在低细胞外镁浓度[Mg2+]o时出现在皮质组织中、频率约为10 Hz的同步爆发活动的机制。我们假设这种活动是持续性的，即与静止状态共存且依赖于缓慢的N-甲基-D-天冬氨酸（NMDA）电导。为了探究这一假设，我们构建并研究了一个基于电导的兴奋性皮质网络模型。群体爆发活动在NMDA衰减时间常数的生理值（约100毫秒）时可以持续存在。神经元在爆发的时间尺度上是同步的，但在单个动作电位的时间尺度上并非如此。一个与自身耦合的细胞的简化模型可以涵盖这种高度同步的网络行为的大部分内容，并使用快慢方法进行分析。如果NMDA电导不太迅速，对于NMDA电导g(NMDA)的中间值会出现同步爆发。对于更大的g(NMDA)会出现规则的动作电位发放活动。如果单细胞是一个条件性爆发细胞，持续性同步爆发会变得更加稳健。对于零AMPA电导g(AMPA)会出现弱同步状态。增强g(AMPA)会增加同步性以及爆发内的动作电位数量，并降低爆发频率。然而，g(AMPA)过强会阻止这种活动，因为它增强了神经元的内在适应性。当[Mg2+]o增加时，需要更高的g(NMDA)值来维持爆发活动。爆发频率随[Mg2+]o降低，并且在生理[Mg2+]o时网络是沉默的。如果抑制性细胞接收到足够的NMDA介导的兴奋，抑制会微弱地降低爆发频率。本研究解释了V层中条件性爆发细胞在低[Mg2+]o时支持癫痫样活动中的重要性。
