Fisher R S, Pedley T A, Moody W J, Prince D A
Arch Neurol. 1976 Feb;33(2):76-83. doi: 10.1001/archneur.1976.00500020004002.
It has been proposed that the notable capacity for epileptogenesis in the hippocampus may be related to potassium accumulation in extracellular spaces. To investigate this hypothesis more directly, we measured changes in extracellular potassium concentration ([K+]o) during focal hippocampal epilepsy using potassium-sensitive microelectrodes. Interictal and ictal electroencephalographic events were accompanied by increases in [K+]o that varied systematically with depth from the ependymal surface and lateral distance from the focus. Maximal [K+]o changes during interictal and ictal discharges occurred in the stratum pyramidale. Initiation of ictal activity did not correlate with a particular "threshold" [K+]o. Comparing these results with similar data from neocortex, we observed that interictal K+ responses in hippocampus lasted longer and had slower rise times, and that peak interictal and ictal [K+]o values were consistently lower. Increases in [K+]o cannot be the sole explanation for regional variations in seizure susceptibility, interictal-ictal transitions, or termination of ictal episodes.
有人提出,海马体中显著的癫痫发生能力可能与细胞外空间的钾离子积累有关。为了更直接地研究这一假设,我们使用钾敏感微电极测量了局灶性海马癫痫发作期间细胞外钾离子浓度([K+]o)的变化。发作间期和发作期的脑电图事件伴随着[K+]o的增加,其随距室管膜表面的深度和距病灶的横向距离而系统变化。发作间期和发作期放电期间最大的[K+]o变化发生在锥体细胞层。发作期活动的起始与特定的“阈值”[K+]o无关。将这些结果与来自新皮层的类似数据进行比较,我们观察到海马体发作间期的钾离子反应持续时间更长,上升时间更慢,并且发作间期和发作期的[K+]o峰值始终更低。[K+]o的增加不能作为癫痫发作易感性、发作间期-发作期转变或发作期终止区域差异的唯一解释。