In vivo models of cortical acquired epilepsy.
In vivo models of cortical acquired epilepsy.
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DOI：
10.1016/j.jneumeth.2015.08.030
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发表时间：
2016-02-15
影响因子：
3
通讯作者：
Timofeev I
中科院分区：
文献类型：
--
作者：
Chauvette S;Soltani S;Seigneur J;Timofeev I
新皮层是几种获得性癫痫的起源部位。在这里，我们简要回顾了最近发展起来的用于研究新皮层癫痫发生的实验模型以及用这些方法获得的一些主要结果。大多数新皮层癫痫发作似乎是在夜间发生的，众所周知，在慢波睡眠期间，神经元活动显示出高度同步性。因此，我们首先介绍神经元同步的机制和同步的正常和病理活动的主要形式。然后，我们描述了三种癫痫发作和癫痫发生的实验模型：氯胺酮-二嗪麻醉作为猫癫痫发作的触发因素，皮质损伤作为皮质穿透伤模型和新皮质点燃模型。除了描述这些模型的具体技术细节外，我们还提供了癫痫发生和癫痫发作期间记录的病理脑活动的主要特征。所有新皮层癫痫发生模型的最共同特征是网络沉默状态持续时间增加，从而上调神经元兴奋性并最终导致癫痫。
The neocortex is the site of origin of several forms of acquired epilepsy. Here we provide a brief review of experimental models that were recently developed to study neocortical epileptogenesis as well as some major results obtained with these methods. Most of neocortical seizures appear to be nocturnal and it is known that neuronal activities reveal high levels of synchrony during slow-wave sleep. Therefore, we start the review with a description of mechanisms of neuronal synchronization and major forms of synchronized normal and pathological activities. Then, we describe three experimental models of seizures and epileptogenesis: ketamine-xylazine anesthesia as feline seizure triggered factor, cortical undercut as cortical penetrating wound model and neocortical kindling. Besides specific technical details describing these models we also provide major features of pathological brain activities recorded during epileptogenesis and seizures. The most common feature of all models of neocortical epileptogenesis is the increased duration of network silent states that up-regulates neuronal excitability and eventually leads to epilepsy.