Neuronal desynchronization as a trigger for seizure generation.
Neuronal desynchronization as a trigger for seizure generation.
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神经元去同步化作为癫痫发作的触发因素。
DOI：
10.1109/tnsre.2007.911084
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Mogul,DavidJ
中科院分区：
文献类型：
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作者：
Li,Yue;Fleming,IoanaNicolaescu;Colpan,MustafaEfkan;Mogul,DavidJ
实验报告挑战了癫痫发作是神经元过度同步的结果这一教条。我们试图探索神经元放电不同步的机制可能诱发癫痫发作。构建了哺乳动物海马切片制备中连接的计算机模型，包括两个最近报道的不同的抑制反馈电路。当中间神经元对锥体树突上的突触的抑制减少时，在 CA3 区域观察到高度局部的癫痫样爆发，类似于在 GABA 能阻断下实验发生的情况。相反，当中间神经元对轴体区域突触的抑制类似地减少时，没有观察到这种爆发。然而，当这种短暂的抑制增加时，正常的协调性兴奋传播就会被高频局部癫痫样爆发打断。这种抑制输入的增加导致锥体神经元的细胞耦合减少。最初观察到相位相干性降低，直到癫痫样活动开始导致相干性净增加，正如在癫痫患者中观察到的那样。这些结果提供了一种可能的途径，其中同步性的降低可以触发诱发癫痫样活动。
Experimental reports have appeared which challenge the dogma that epileptic seizures arise as a consequence of neuronal hypersynchronization. We sought to explore what mechanisms that desynchronize neuronal firing could induce epileptic seizures. A computer model of connections in a mammalian hippocampal slice preparation was constructed including two recently-reported distinct inhibitory feedback circuits. When inhibition by interneurons that synapse on pyramidal dendrites was decreased, highly localized seizure-like bursting was observed in the CA3 region similar to that which occurs experimentally under GABAergic blockade. In contrast, when inhibition by interneurons that synapse in the axosomatic region was similarly decreased, no such bursting was observed. However, when this transient inhibition was increased, normal coordinated spread of excitation was interrupted by high-frequency localized seizure-like bursting. The increase of this inhibitory input resulted in decreased cell coupling of pyramidal neurons. A decrease in phase coherence was initially observed until seizure-like activity initiated causing a net increase in coherence as has been observed in epileptic patients. These results provide a possible pathway in which a decrease in synchronization could provide the trigger for inducing epileptiform activity.