Department of Anatomy, Faculty of Medicine of University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal.
Behav Brain Res. 2011 Dec 1;225(2):538-46. doi: 10.1016/j.bbr.2011.07.057. Epub 2011 Aug 5.
Prolonged seizures produce death of hippocampal neurons, which is thought to initiate epileptogenesis and cause a disruption of hippocampally mediated behaviors. This study aimed to evaluate behavioral and neuroanatomical changes induced by brief seizures and to compare them with changes induced by prolonged seizures. Adult rats were administered 6 brief seizures, elicited by electroshock (ECS). Prolonged seizures (status epilepticus, SE) were induced by pilocarpine. Two months later, the rats' behavior was tested using the Morris water maze, passive avoidance and active avoidance tests. The number of neurons in the hippocampal formation was estimated using stereological methods. ECS seizures produced loss of neurons, ranging between 14% and 26%, in the dentate hilus, subiculum, presubiculum, parasubiculum, and entorhinal layers III and V/VI. However, the neuron loss caused by SE in the same structures, as well as in the hippocampal CA3 and CA1 fields, ranged between 34% and 50%. SE additionally killed many neurons in the dentate granular layer, postsubiculum and entorhinal layer II. ECS treatment caused mild impairments in spatial learning and passive avoidance, but it was not associated with spontaneous motor seizures. In contrast, SE produced a severe disruption of spatial learning, passive and active avoidance, and led to the development of spontaneous seizures. These data show that both prolonged seizure activity and brief seizures result in structural and functional alterations in the temporal lobe circuits, but those caused by prolonged seizures are considerably more severe. Hippocampal damage elicited by brief seizures does not necessarily lead to spontaneous motor seizures.
癫痫发作持续时间过长会导致海马神经元死亡，这被认为是癫痫发生的起始原因，并导致海马介导的行为中断。本研究旨在评估短暂性癫痫发作引起的行为和神经解剖学变化，并将其与持续性癫痫发作引起的变化进行比较。成年大鼠接受电休克（ECS）诱发的 6 次短暂性癫痫发作。通过匹罗卡品诱导癫痫持续状态（SE）。两个月后，使用 Morris 水迷宫、被动回避和主动回避测试评估大鼠的行为。使用体视学方法估计海马结构中的神经元数量。ECS 癫痫发作导致齿状回、下托、前下托、副下托和内嗅皮层 III 和 V/VI 层中的神经元损失 14%-26%。然而，SE 在相同结构以及海马 CA3 和 CA1 场中引起的神经元损失范围在 34%-50%之间。SE 还杀死了齿状回颗粒层、后下托和内嗅皮层 II 中的许多神经元。ECS 治疗导致空间学习和被动回避轻度受损，但与自发性运动性癫痫无关。相比之下，SE 导致空间学习、被动和主动回避严重障碍，并导致自发性癫痫发作的发展。这些数据表明，持续时间较长的癫痫发作活动和短暂性癫痫发作都会导致颞叶回路的结构和功能改变，但持续时间较长的癫痫发作引起的改变更为严重。短暂性癫痫发作引起的海马损伤不一定导致自发性运动性癫痫。
