Department of Neurology and Regional Epilepsy Center, University of Washington, Seattle, Washington 98104, USA.
Epilepsia. 2012 Dec;53 Suppl 9(Suppl 9):32-40. doi: 10.1111/epi.12033.
Ion channel dysfunction or "channelopathy" is a proven cause of epilepsy in the relatively uncommon genetic epilepsies with Mendelian inheritance. But numerous examples of acquired channelopathy in experimental animal models of epilepsy following brain injury have also been demonstrated. Our understanding of channelopathy has grown due to advances in electrophysiology techniques that have allowed the study of ion channels in the dendrites of pyramidal neurons in cortex and hippocampus. The apical dendrites of pyramidal neurons comprise the vast majority of neuronal surface membrane area, and thus the majority of the neuronal ion channel population. Investigation of dendritic ion channels has demonstrated remarkable plasticity in ion channel localization and biophysical properties in epilepsy, many of which produce hyperexcitability and may contribute to the development and maintenance of the epileptic state. Herein we review recent advances in dendritic physiology and cell biology, and their relevance to epilepsy.
离子通道功能障碍或“通道病”是具有孟德尔遗传的相对罕见遗传性癫痫的已知病因。但在脑损伤后的癫痫实验动物模型中，也已经证实了许多获得性通道病的例子。由于电生理学技术的进步，我们对通道病的理解也得到了提高，这些技术使我们能够研究皮质和海马锥体神经元树突中的离子通道。锥体神经元的树突构成了绝大多数神经元细胞膜表面积，因此也是大多数神经元离子通道群体的所在。对树突离子通道的研究表明，在癫痫中离子通道定位和生物物理特性具有显著的可变性，其中许多特性会产生过度兴奋，可能有助于癫痫状态的发展和维持。本文综述了树突生理和细胞生物学的最新进展及其与癫痫的相关性。
