Setkowicz Zuzanna, Nowak Barbara, Janeczko Krzysztof
Department of Neuroanatomy, Institute of Zoology, Jagiellonian University, 6 Ingardena St., 30 060 Kraków, Poland.
Epilepsy Res. 2006 Mar;68(3):255-63. doi: 10.1016/j.eplepsyres.2005.11.012. Epub 2006 Jan 18.
Gliosis, axonal sprouting and remodelling of nerve connections in the injured brain have been regarded as epileptogenic processes dependent on the age when the injury was inflicted. The present study examines whether brains injured at different developmental stages may acquire different susceptibility to experimental status epilepticus induced in adulthood. In 6- and 30-day-old Wistar rats (P6s and P30s, respectively), a mechanical injury was performed in the left cerebral hemisphere. On postnatal day 60, all the animals and controls received single injections of kainic acid to evoke status epilepticus. During a 6-h period following the injection, the animals were observed continuously and motor symptoms of seizure activity were recorded and rated. P6s showed significantly lower intensity of kainic acid-induced epileptic symptoms and significantly longer survival than controls or P30s. In P30s, no significant change was detected. The data provide evidence that the developmental stage when the brain is injured determines epileptogenecity of the lesion. However, a considerable discrepancy between these data and those obtained previously following pilocarpine administration in the same experimental models of brain injury shows that each of the two models of epilepsy may display different aspects of the same age-dependent process triggered by the brain injury.
脑损伤后胶质增生、轴突发芽和神经连接重塑被认为是与损伤发生时年龄相关的致痫过程。本研究探讨了在不同发育阶段受伤的大脑在成年后对实验性癫痫持续状态是否具有不同的易感性。在6日龄和30日龄的Wistar大鼠(分别为P6和P30)中,对左侧大脑半球进行机械损伤。在出生后第60天,所有动物和对照组均单次注射 kainic 酸以诱发癫痫持续状态。在注射后的6小时内,持续观察动物,并记录和评估癫痫发作活动的运动症状。P6组 kainic 酸诱导的癫痫症状强度显著低于对照组或P30组,且存活时间显著长于对照组或P30组。在P30组中,未检测到显著变化。这些数据表明,脑损伤时的发育阶段决定了损伤的致痫性。然而,这些数据与之前在相同脑损伤实验模型中给予毛果芸香碱后获得的数据之间存在相当大的差异,这表明两种癫痫模型中的每一种可能都展示了由脑损伤引发的相同年龄依赖性过程的不同方面。