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癫痫是最常见的神经系统疾病之一,临床主要表现为周期性和无法预见性的癫痫样发作。目前认为,癫痫的形成、同步化以及癫痫样放电的维持与细胞间的缝隙连接有关。大量的体内外实验研究表明,缝隙连接抑制剂具有较强的抗癫痫作用,提示缝隙连接可能成为开发新型抗癫痫药物的潜在靶点。此外,选择性药理学研究和基因敲除技术研究表明,神经元间与胶质细胞间的缝隙连接在癫痫中的作用需区别看待。随着条件性基因敲除技术的成熟、高选择性的新型缝隙连接调控药物的出现以及更详细的人类癫痫脑组织样本的研究,人们将更全面地了解缝隙连接在癫痫中的作用。本综述总结了目前关于缝隙连接在癫痫发病机制中作用的研究结果,并对临床和基础研究中癫痫发作导致的缝隙连接蛋白表达的变化进行讨论。
Epilepsy is one of the most common neurological diseases, the clinical manifestations of cyclical and unpredictable epilepsy. It is currently believed that the formation of epilepsy, synchronization and maintenance of epileptiform discharges and the gap between the cells connected. A large number of in vitro and in vivo studies have shown that gap junction inhibitors have a strong anti-epileptic effect, suggesting that gap junction may be a potential target for the development of novel antiepileptic drugs. In addition, selective pharmacological studies and gene knockout studies indicate that the role of gap junctions between neurons and glial cells in epilepsy needs to be differentiated. With the development of conditional gene knockout technology, the emergence of new and highly selective new gap junction modulating drugs, and more detailed studies of human epilepsy brain tissue samples, one will gain a more complete understanding of the role of gap junction in epilepsy. This review summarizes current findings on the role of gap junction in the pathogenesis of epilepsy and discusses the changes in the expression of gap junction protein in seizures in clinical and basic research.