Epileptogenesis in the developing brain: What can we learn from animal models?
Epileptogenesis in the developing brain: What can we learn from animal models?
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DOI：
10.1111/j.1528-1167.2007.01281.x
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发表时间：
2007-01-01
期刊：
影响因子：
5.6
通讯作者：
Baram, Tallie Z.
中科院分区：
文献类型：
--
作者：
Bender, Roland A.;Baram, Tallie Z.
关于癫痫产生过程（癫痫发生）的知识还不完整，并且一直是主要研究工作的主题。动物模型可以告诉我们这些过程。我们关注发育中大脑中癫痫发生的显着特征，并建立与人类颞叶癫痫相关的长时间热性惊厥 (FS) 模型。在 FS 动物模型中，大约 35% 的大鼠发生癫痫发生。与大多数成人获得性癫痫发作不同，生命早期的这一过程（在热性惊厥模型以及其他几种模型中）不需要“损伤”（细胞死亡）。相反，生命早期的癫痫发生涉及分子机制，包括癫痫诱发的受体和离子通道表达的长期改变。虽然基因表达程序的短暂变化在生命早期癫痫发作后很常见，但持久的影响（例如实验性 FS 后发现的结果）与癫痫发生有关。 FS 产生持久的分子变化和癫痫的能力表明，包括 FS 生成固有的细胞因子激活在内的机制也可能在这些癫痫发作的致癫痫后果中发挥作用。
Knowledge of the processes by which epilepsy is generated (epileptogenesis) is incomplete and has been a topic of major research efforts. Animal models can inform us about these processes. We focus on the distinguishing features of epileptogenesis in the developing brain and model prolonged febrile seizures (FS) that are associated with human temporal lobe epilepsy. In the animal model of FS, epileptogenesis occurs in similar to 35% of rats. Unlike the majority of acquired epileptogeneses in adults, this process early in life (in the febrile seizures model as well as in several others) does not require "damage" (cell death). Rather, epileptogenesis early in life involves molecular mechanisms including seizure-evoked, long-lasting alterations of the expression of receptors and ion channels. Whereas transient changes in gene expression programs are common after early-life seizures, enduring effects, such as found after experimental FS, are associated with epileptogenesis. The ability of FS to generate long-lasting molecular changes and epilepsy suggests that mechanisms, including cytokine activation that are intrinsic to FS generation, may play a role also in the epileptogenic consequences of these seizures.