Department of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Neurobiol Dis. 2012 Jan;45(1):348-55. doi: 10.1016/j.nbd.2011.08.020. Epub 2011 Aug 25.
Seizures may directly cause brain injury by disrupting the structure and function of synapses. Previous studies using in vivo time-lapse imaging have demonstrated an acute beading of dendrites and loss of dendritic spines immediately following status epilepticus, but the effects of brief seizures and the long-term evolution of this dendritic injury are unknown. Here, we examined the effects of seizures of varying durations on dendritic structure over several weeks using in vivo multiphoton imaging with kainate-induced seizures in mice. The degree of dendritic injury was directly dependent on the duration of the seizures, with seizures lasting more than 30 min (status epilepticus) resulting in a greater than 75% spine loss. However, even brief seizures (<5 min) induced moderate dendritic beading and spine loss. The dendritic injury from brief seizures usually recovered within 2 weeks, whereas status epilepticus-induced injury only partially reversed. These studies demonstrate that seizures of all durations may trigger at least transient neuronal injury.
癫痫发作可能通过破坏突触的结构和功能而直接导致脑损伤。先前使用活体延时成像的研究表明,在癫痫持续状态后,树突会立即出现急性珠状改变和树突棘丢失,但短暂性癫痫发作的影响和这种树突损伤的长期演变尚不清楚。在这里,我们使用活体多光子成像研究了不同持续时间的癫痫发作对树突结构的影响,使用海人酸诱导的癫痫发作在小鼠中进行。树突损伤的程度与癫痫发作的持续时间直接相关,持续时间超过 30 分钟(癫痫持续状态)会导致超过 75%的棘突丢失。然而,即使是短暂的癫痫发作(<5 分钟)也会引起中度的树突珠状改变和棘突丢失。短暂性癫痫发作引起的树突损伤通常在 2 周内恢复,而癫痫持续状态引起的损伤仅部分逆转。这些研究表明,所有持续时间的癫痫发作都可能引发至少是短暂的神经元损伤。