Wu Y, Liu D, Song Z
The Neurology Department of Third Xiangya Hospital, Medical School of Central South University, Changsha, China.
The Neurology Department of Third Xiangya Hospital, Medical School of Central South University, Changsha, China.
Neuroscience. 2015 Feb 26;287:175-86. doi: 10.1016/j.neuroscience.2014.06.046. Epub 2014 Jun 30.
Epilepsy can be defined as the abnormal activities of neurons. The occurrence, propagation and termination of epileptic seizures rely on the networks of neuronal cells that are connected through both synaptic- and non-synaptic interactions. These complicated interactions contain the modified functions of normal neurons and glias as well as the mediation of excitatory and inhibitory mechanisms with feedback homeostasis. Numerous spread patterns are detected in disparate networks of ictal activities. The cortical-thalamic-cortical loop is present during a general spike wave seizure. The thalamic reticular nucleus (nRT) is the major inhibitory input traversing the region, and the dentate gyrus (DG) controls CA3 excitability. The imbalance between γ-aminobutyric acid (GABA)-ergic inhibition and glutamatergic excitation is the main disorder in epilepsy. Adjustable negative feedback that mediates both inhibitory and excitatory components affects neuronal networks through neurotransmission fluctuation, receptor and transmitter signaling, and through concomitant influences on ion concentrations and field effects. Within a limited dynamic range, neurons slowly adapt to input levels and have a high sensitivity to synaptic changes. The stability of the adapting network depends on the ratio of the adaptation rates of both the excitatory and inhibitory populations. Thus, therapeutic strategies with multiple effects on seizures are required for the treatment of epilepsy, and the therapeutic functions on networks are reviewed here. Based on the high-energy burst theory of epileptic activity, we propose a potential antiepileptic therapeutic strategy to transfer the high energy and extra electricity out of the foci.
癫痫可被定义为神经元的异常活动。癫痫发作的发生、传播和终止依赖于通过突触和非突触相互作用连接的神经元细胞网络。这些复杂的相互作用包括正常神经元和神经胶质细胞功能的改变，以及具有反馈稳态的兴奋性和抑制性机制的介导。在不同的发作期活动网络中检测到多种传播模式。在全身性棘波发作期间存在皮质 - 丘脑 - 皮质环路。丘脑网状核（nRT）是穿过该区域的主要抑制性输入，而齿状回（DG）控制CA3的兴奋性。γ-氨基丁酸（GABA）能抑制和谷氨酸能兴奋之间的失衡是癫痫的主要紊乱。介导抑制性和兴奋性成分的可调节负反馈通过神经传递波动、受体和递质信号传导，以及通过对离子浓度和场效应的伴随影响来影响神经元网络。在有限的动态范围内，神经元会缓慢适应输入水平，并对突触变化具有高敏感性。适应性网络的稳定性取决于兴奋性和抑制性群体的适应率之比。因此，治疗癫痫需要具有多种抗癫痫作用的治疗策略，本文将对网络上的治疗功能进行综述。基于癫痫活动的高能爆发理论，我们提出了一种潜在的抗癫痫治疗策略，即将高能量和多余的电从病灶中转移出去。
