Abstract

Epilepsy is one of the prevalent cerebral diseases, and despite intensive research of this pathology for many years, modern medicine cannot effectively control seizure manifestations in almost a third of patients. In epilepsy, there is a reorganization of neural networks, which is the result of the death of some neurons and the formation of new neuronal connections with altered properties. In this review, we focused on the analysis of changes in the properties of a key element of neural networks, the chemical synapse, immediately after epileptic activity, during epileptogenesis, and in chronic epilepsy. Since the synapse includes not only neuronal pre- and postsynaptic parts, but also glial components, our consideration includes changes in the properties of astrocytes and microglia. Epileptic activity causes numerous modifications in synapse function: changes in the probability of mediator release, the alteration of subunit composition of postsynaptic receptors, impairments of synaptic plasticity, and changes in morphology and activity of astrocytes and microglia. Glial cells release several gliatransmitters and cytokines, which in turn modify synaptic transmission. In some cases, the combination of these changes is favorable and allows compensating almost completely the consequences of epileptic activity for the nervous system. However, quite often, these changes, on the contrary, trigger a cascade of events leading to epilepsy and long-term disturbances in the functioning of neural networks. Over the past 10 years, significant progress has been achieved in deciphering these changes and their mechanisms, which is covered in our review. However, until now, researchers have not yet reached consensus on which particular modifications in the functioning of synapses provide optimal compensation and are able to prevent epileptogenesis. This knowledge could be the basis for the development of effective methods for epileptogenesis prevention and epilepsy treatment.

中文翻译：

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癫痫的突触功能障碍

摘要

癫痫是常见的脑部疾病之一，尽管多年来对该病理学进行了深入研究，但现代医学无法有效控制近三分之一患者的癫痫发作表现。在癫痫症中，神经网络会发生重组，这是一些神经元死亡和具有改变特性的新神经元连接形成的结果。在这篇综述中，我们重点分析了神经网络的一个关键元素化学突触的特性变化，即癫痫活动后、癫痫发生期间和慢性癫痫。由于突触不仅包括神经元突触前和突触后部分，还包括神经胶质成分，我们的考虑包括星形胶质细胞和小胶质细胞特性的变化。癫痫活动会导致突触功能发生许多变化：介质释放概率的变化、突触后受体亚基组成的改变、突触可塑性受损以及星形胶质细胞和小胶质细胞的形态和活性变化。神经胶质细胞释放多种神经胶质递质和细胞因子，进而改变突触传递。在某些情况下，这些变化的组合是有利的，可以几乎完全补偿癫痫活动对神经系统的影响。然而，相反，这些变化往往会引发一系列事件，导致癫痫和神经网络功能的长期紊乱。在过去的 10 年里，在破译这些变化及其机制方面取得了重大进展，我们的评论中涵盖了这一点。然而，到目前为止，研究人员尚未就突触功能的哪些特定修饰提供最佳补偿并能够预防癫痫发生达成共识。这些知识可能是开发有效的癫痫发生预防和癫痫治疗方法的基础。