Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, China.
Neurodegenerative Disease Research Program, Sanford-Burnham Medical Research Institute, La Jolla, CA, United States.
Front Neural Circuits. 2018 Jun 29;12:48. doi: 10.3389/fncir.2018.00048. eCollection 2018.
Epilepsy is one of the most common neurological disorders affecting millions of people. Due to the complicated and unclear mechanisms of epilepsy, still a significant proportion of epilepsy patients remain poorly controlled. Epilepsy is characterized by convulsive seizures that are caused by increased excitability. In this study, by using kainic acid (KA)-induced epilepsy mice, we investigated the neuronal activities and revealed the neuronal compensatory mechanisms after KA-induced toxic hyperexcitability. The results indicate that both phasic inhibition induced by enhanced inhibitory synaptic activity and tonic inhibition mediated by activated astrocytes participate in the compensatory mechanisms. Compensatory mechanisms were already found in various neuronal disorders and were considered important in protecting nervous system from toxic hyperexcitability. This study hopefully will provide valuable clues in understanding the complex neuronal mechanisms of epilepsy, and exploring potential clinical treatment of the disease.
癫痫是影响数百万人的最常见神经系统疾病之一。由于癫痫的机制复杂且不明确，仍有相当一部分癫痫患者的病情控制不佳。癫痫的特征是由兴奋性增加引起的惊厥性发作。在这项研究中，我们使用海人酸（KA）诱导的癫痫小鼠，研究了神经元活动，并揭示了 KA 诱导的毒性过度兴奋后的神经元补偿机制。结果表明，增强的抑制性突触活动引起的相性抑制和激活的星形胶质细胞介导的紧张性抑制都参与了补偿机制。补偿机制在各种神经元疾病中都有发现，被认为对保护神经系统免受毒性过度兴奋很重要。本研究有望为理解癫痫的复杂神经元机制提供有价值的线索，并探索该疾病的潜在临床治疗方法。
