Wong R K, Traub R D, Miles R
Adv Neurol. 1986;44:583-92.
Synchronized discharge of populations of cortical neurons are often observed to underly both the interictal spikes and tonic seizures generated in experimental epilepsy studies. Recently it has been shown that similar synchronized discharges occur in cortical brain slices treated with convulsants such as penicillin, picrotoxin, or bicuculline. The favorable experimental conditions offered by the in vitro preparation have facilitated a detailed examination on the cellular basis for the generation of the epileptic neuronal synchrony. In this chapter we shall review some experimental observations on the neuronal synchronization and describe a mechanism for its generation based on the computer simulation approach. Three factors are considered to be essential for epileptic synchronization observation in vitro. First, cortical neurons may intrinsically generate bursts of action potentials. Second, recurrent excitatory connections exist that are sufficiently powerful that bursting activity may spread between synaptically connected neurons. Third, inhibition within the local neuronal circuit must be adequately attenuated to allow excitation to spread through the recurrent excitatory connections. Computer simulation studies have been based on these assumptions, using neuronal networks where each cell is connected to more than one postsynaptic neuron. Bursting initiated in one cell excites all its follower cells, and the sequential recruitment of an increasing number of cells eventually leads to a simultaneous discharge of the population. A number of recent experimental observations lend credence to the proposed scheme for neuronal synchrony. Simultaneous paired intracellular recordings provided direct evidence that a burst of action potentials in a presynaptic cell can activate action potentials postsynaptically. Furthermore, it is shown that the rhythm of spontaneous discharge in a neuronal population can be influenced by the activity of one neuron within the population.
在实验性癫痫研究中,经常观察到皮质神经元群的同步放电是发作间期棘波和强直性癫痫发作的基础。最近研究表明,在用惊厥剂(如青霉素、印防己毒素或荷包牡丹碱)处理的皮质脑片中也会出现类似的同步放电。体外实验所提供的良好实验条件有助于在细胞层面详细研究癫痫神经元同步化的产生机制。在本章中,我们将回顾一些关于神经元同步化的实验观察结果,并基于计算机模拟方法描述其产生机制。体外癫痫同步化观察中,有三个因素被认为是必不可少的。第一,皮质神经元可能内在地产生动作电位爆发。第二,存在足够强大的反复性兴奋性连接,使得爆发活动能够在突触连接的神经元之间传播。第三,局部神经元回路内的抑制作用必须充分减弱,以使兴奋能够通过反复性兴奋性连接传播。计算机模拟研究基于这些假设,使用每个细胞都与不止一个突触后神经元相连的神经网络。一个细胞引发的爆发会激发其所有后续细胞,随着越来越多的细胞被依次激活,最终导致整个神经元群同时放电。最近的一些实验观察结果支持了所提出的神经元同步化机制。同时进行的双细胞内记录提供了直接证据,表明突触前细胞的动作电位爆发能够在突触后激活动作电位。此外,研究表明神经元群中自发放电的节律会受到群体内单个神经元活动的影响。