Characterization of developing rat cortical neurons after epileptiform discharges
Characterization of developing rat cortical neurons after epileptiform discharges
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DOI：
10.1016/j.ijdevneu.2010.06.006
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发表时间：
2010-10-01
影响因子：
1.8
通讯作者：
Jiang, Yuwu
中科院分区：
文献类型：
--
作者：
Jiang, Qian;Wu, Ye;Jiang, Yuwu
发育中的大脑经历了重大的重组，以应对早期的环境变化。新生儿大脑快速发育的兴奋程度提高，也使其极易受到年龄特异性癫痫发作的影响，这可能导致终身的认知和神经功能障碍。然而，目前尚不清楚癫痫发作如何干扰发育程序以及癫痫发生如何实现。在这里，通过使用体外模型，我们报告了癫痫样活动诱导后皮质细胞的全球异常状态：更多的NR 2B靶向神经元表面，NR 2A较少。树木毒性包括树枝状串珠，扭曲和简化的树枝分支模式。早期生活中的神经元样损伤也对兴奋性突触的大小和PSD-95与NR 2A或NR 2B受体亚单位之间的相互作用产生影响。我们的研究结果支持异常发育，或者更糟的是，类似于未成熟细胞的细胞变性，这可能会更好地理解早期癫痫发作及其相关损伤的病理机制。(C)2010 ISDN。由爱思唯尔有限公司出版。保留所有权利。
The developing brain undergoes major reorganization in response to early environmental changes. The elevated excitation that allows the neonatal brain to develop quickly also makes it highly vulnerable to age-specific seizures that can cause lifelong cognitive and neurological disability. However, it is not yet clear how seizures interfere with the developmental program and how epileptogenesis actualize. Here, by using an in vitro model, we report a global abnormal status of cortical cells after epileptiform activity was induced: more NR2B is targeted on the neuronal surface with less NR2A. Dendrotoxicity including dendritic beading, distortion and simplification of dendritic branching patterns were observed. Early-life seizure-like insults also exert effects on the excitatory synaptic size and interactions between PSD-95 and NR2A or NR2B receptor subunits. Our findings support an abnormal development or, worse, cellular degeneration that resembles immature cells, which may enlighten better understanding of the pathological mechanism of early-life seizures and its related injury. (C) 2010 ISDN. Published by Elsevier Ltd. All rights reserved.