Godukhin O V
Institute of Theoretical and Experimental Biophysics of Russian Academy of Sciences, Pushchino, Moscov Region.
Usp Fiziol Nauk. 2005 Apr-Jun;36(2):41-54.
Kindling is a phenomenon in which repeated application of an initially subcunvulsive stimulus to the certain sites of the brain results in progressive reduction of the threshold for induction of seizure activity. Following its discovery, kindling became a one of the major focus of neuruscientific investigations because of the similarities between this phenomenon and the progressive development of human epilepsy after head injury. However, kindling is not only the model of epileptogenesis but is considered as the model of activity-dependent form of neuroplasticity which is responsible for the development of cellular-molecular and network events producing the dicordered firing of subpopulations of neurons. Although kindling is fundamentally a network phenomenon, the most basic manifestation of the hyperexcitability characteristic of kindling can be evident at the level of a single neuron. The purpose of the present review is to integrate the data obtained recently about an involvement of voltage-dependent membrane channels, synaptic processed, second messenger systems and transcription factors in the cellular-molecular mechanisms leading to the induction, spreading and maintenance of seizure activity during kindling. The relationships between long-term potentiation and kindling model of epileptogenesis are also discussed.
点燃效应是一种现象，即对大脑特定部位反复施加最初亚惊厥性刺激会导致癫痫发作活动诱导阈值的逐渐降低。自其被发现以来，点燃效应因其与人类头部受伤后癫痫的渐进性发展相似，成为神经科学研究的主要焦点之一。然而，点燃效应不仅是癫痫发生的模型，还被视为依赖活动形式的神经可塑性模型，这种神经可塑性负责产生神经元亚群无序放电的细胞分子和网络事件的发展。尽管点燃效应从根本上说是一种网络现象，但点燃效应超兴奋性特征的最基本表现可以在单个神经元水平上显现出来。本综述的目的是整合最近获得的关于电压依赖性膜通道、突触过程、第二信使系统和转录因子参与点燃效应期间癫痫发作活动的诱导、传播和维持的细胞分子机制的数据。还讨论了长时程增强与癫痫发生的点燃效应模型之间的关系。
