Gjerstad L, Andersen P, Langmoen I A, Lundervold A, Hablitz J
Acta Physiol Scand. 1981 Oct;113(2):245-52. doi: 10.1111/j.1748-1716.1981.tb06890.x.
Intra- and extracellular recordings were made in the transverse hippocampal slice in vitro to study the requirements for the triggering of epileptiform discharges of CA1 cells. Spontaneous and induced epileptiform discharges were produced by adding small amounts of sodium benzyl penicillin. Recorded intracellularly, the epileptiform activity consisted of a burst of action potentials superimposed on a depolarizing wave. Extracellular recordings demonstrated a marked synchronization. The epileptiform activity of the CA1 cells appeared without changes in the passive membrane properties or in the spike generating mechanism. Spontaneous epileptiform discharges of the CA2 cells depended upon a synaptic activation from the CA3 region. Stimulation of afferent fibres evoked an early and a late burst response in the CA2 cells. The long latency burst was caused by a re-excitation from the CA3 region. The early burst response seems to be an intrinsic property of the CA1 cells and may be induced by synaptic activation of either apical or basal dendrites. The findings suggest that synaptic depolarization is necessary for the generation of epileptiform discharges of the CA1 cells.
在体外横向海马切片中进行细胞内和细胞外记录,以研究触发CA1细胞癫痫样放电的条件。通过添加少量苄青霉素钠产生自发性和诱发性癫痫样放电。细胞内记录显示,癫痫样活动由叠加在去极化波上的一串动作电位组成。细胞外记录显示出明显的同步性。CA1细胞的癫痫样活动在被动膜特性或动作电位产生机制方面没有变化。CA2细胞的自发性癫痫样放电依赖于来自CA3区域的突触激活。刺激传入纤维在CA2细胞中诱发早期和晚期爆发反应。长潜伏期爆发是由CA3区域的再次兴奋引起的。早期爆发反应似乎是CA1细胞的固有特性,可能由顶树突或基底树突的突触激活诱导。这些发现表明,突触去极化是CA1细胞产生癫痫样放电所必需的。