Jensen M S, Yaari Y
Institute of Physiology, Aarhus University, Denmark.
Ann Neurol. 1988 Nov;24(5):591-8. doi: 10.1002/ana.410240502.
In studies of focal epilepsy it is frequently assumed that the interictal spike is the elementary form of epileptic activity and that seizure, or ictal, episodes evolve by temporal summation and spatial expansion of interictal paroxysms. We examined this hypothesis in an in vitro model of acute focal epilepsy produced by perfusing rat hippocampal slices with solutions containing moderately elevated concentrations of K+. Some of the preparations treated in this way displayed recurring electrical seizures in the CA1 field. Each seizure episode typically evolved by a seemingly smooth progression of brief interictal bursts into sustained ictal discharge. However, exposure of preparations showing electrical seizures to blockers of synaptic transmission or to cholinergic agonists abolished interictal spiking in all hippocampal fields but did not impede the initiation of ictal episodes in area CA1. Likewise, severing the connections between areas CA3 and CA1 abolished interictal spiking in area CA1 without disrupting the initiation of seizures in this region. These data clearly show that in this model, focal seizures arise independent of interictal spikes and through different cellular mechanisms. While interictal electrogenesis requires chemical synaptic excitation, ictal episodes can be initiated and maintained by nonsynaptic neuronal interactions.
在局灶性癫痫的研究中，人们常常假定发作间期棘波是癫痫活动的基本形式，并且癫痫发作（即发作期）是由发作间期阵发性活动的时间总和与空间扩展演变而来。我们在一个急性局灶性癫痫的体外模型中检验了这一假说，该模型是通过用含有适度升高浓度钾离子的溶液灌注大鼠海马切片制成的。以这种方式处理的一些标本在CA1区出现了反复的电发作。每次发作通常由短暂的发作间期猝发看似平稳地演变为持续的发作期放电。然而，将出现电发作的标本暴露于突触传递阻滞剂或胆碱能激动剂下，会消除所有海马区的发作间期棘波，但不会阻碍CA1区发作期的起始。同样，切断CA3区和CA1区之间的联系会消除CA1区的发作间期棘波，而不会破坏该区域发作的起始。这些数据清楚地表明，在这个模型中，局灶性发作的出现独立于发作间期棘波，并且通过不同的细胞机制产生。虽然发作间期的电活动需要化学性突触兴奋，但发作期可以由非突触性神经元相互作用起始并维持。
