Toth Z, Yan X X, Haftoglou S, Ribak C E, Baram T Z
Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, California 92697-4475, USA.
J Neurosci. 1998 Jun 1;18(11):4285-94. doi: 10.1523/JNEUROSCI.18-11-04285.1998.
Febrile seizures are the most common seizure type in young children. Whether they induce death of hippocampal and amygdala neurons and consequent limbic (temporal lobe) epilepsy has remained controversial, with conflicting data from prospective and retrospective studies. Using an appropriate-age rat model of febrile seizures, we investigated the acute and chronic effects of hyperthermic seizures on neuronal integrity and survival in the hippocampus and amygdala via molecular and neuroanatomical methods. Hyperthermic seizures-but not hyperthermia alone-resulted in numerous argyrophilic neurons in discrete regions of the limbic system; within 24 hr of seizures, a significant proportion of neurons in the central nucleus of the amygdala and in the hippocampal CA3 and CA1 pyramidal cell layer were affected. These physicochemical alterations of hippocampal and amygdala neurons persisted for at least 2 weeks but were not accompanied by significant DNA fragmentation, as determined by in situ end labeling. By 4 weeks after the seizures, no significant neuronal dropout in these regions was evident. In conclusion, in the immature rat model, hyperthermic seizures lead to profound, yet primarily transient alterations in neuronal structure.
热性惊厥是幼儿最常见的惊厥类型。它们是否会导致海马体和杏仁核神经元死亡以及随之而来的边缘系统（颞叶）癫痫一直存在争议，前瞻性和回顾性研究的数据相互矛盾。我们使用适龄大鼠热性惊厥模型，通过分子和神经解剖学方法研究了高温惊厥对海马体和杏仁核神经元完整性和存活的急性和慢性影响。高温惊厥——而非单纯高热——导致边缘系统离散区域出现大量嗜银神经元；惊厥发作后24小时内，杏仁核中央核以及海马体CA3和CA1锥体细胞层中的很大一部分神经元受到影响。海马体和杏仁核神经元的这些物理化学改变持续了至少2周，但原位末端标记显示并未伴随明显的DNA片段化。惊厥发作后4周，这些区域未出现明显的神经元脱失。总之，在未成熟大鼠模型中，高温惊厥会导致神经元结构发生深刻但主要是短暂的改变。
