Dreier J P, Heinemann U
Institute of Neurophysiology, University at Cologne, Federal Republic of Germany.
Exp Brain Res. 1991;87(3):581-96. doi: 10.1007/BF00227083.
In order to study spatial interactions during low magnesium induced epileptiform activity, changes in extracellular potassium concentration ([K+]0) and associated slow field potentials (f.p.'s) were recorded in thin rat temporal cortex slices (400 microns) containing the neocortical temporal area 3 (Te3), the entorhinal cortex (EC) and the hippocampal formation with the dentate gyrus, area CA3 and CA1 and the subiculum (Sub). The epileptiform activity was characterized by short recurrent epileptiform discharges (40 to 80 ms, 20/min) in areas CA3 and CA1 and by interictal discharges and tonic and clonic seizure like events (SLE's) (13-88s) in the EC, Te3 and Sub. While interictal discharges occurred independent of each other in the different subfields, the three areas became synchronized during the course of a SLE. The EC, Te3 and Sub all could represent the "focus" for generation of the SLE's. This initiation site for SLE's sometimes changed from one area to another. The characteristics of the rises in [K+]0 and subsequent undershoots were comparable to previous observations in in vivo preparations. Interestingly, rises in [K+]0 could start before actual onset of seizure like activity in secondarily recruited areas. The epileptiform activity could change its characteristics to either a state of recurrent tonic discharge episodes or to a continuous clonic discharge state reminiscent of various forms of status epilepticus. We did not observe, in any of these states, active participation by area CA3 in the epileptiform activity of the EC in spite of clear projected activity to the dentate gyrus. Even after application of picrotoxin (20 microM), area CA3 did not actively participate in the SLE's generated in the entorhinal cortex. When baclofen (2 microM) was added to the picrotoxin containing medium, SLE's occurred both in the entorhinal cortex and in area CA3, suggesting that inhibition of inhibitory interneurons by baclofen could overcome the "filtering" of projected activity from the entorhinal cortex to the hippocampus.
为了研究低镁诱导癫痫样活动期间的空间相互作用,在包含新皮质颞叶区域3(Te3)、内嗅皮质(EC)以及具有齿状回、CA3区、CA1区和下托(Sub)的海马结构的薄大鼠颞叶皮质切片(400微米)中记录了细胞外钾离子浓度([K+]0)的变化以及相关的慢场电位(f.p.)。癫痫样活动的特征是CA3区和CA1区出现短暂的反复癫痫样放电(40至80毫秒,每分钟20次),以及EC、Te3和Sub区出现发作间期放电和强直阵挛样发作事件(SLE)(13 - 88秒)。虽然发作间期放电在不同子区域中相互独立发生,但在SLE过程中这三个区域会同步。EC、Te3和Sub都可能是SLE产生的“焦点”。SLE的起始部位有时会从一个区域转移到另一个区域。[K+]0升高及随后的负后电位的特征与先前在体内实验中的观察结果相似。有趣的是,在继发募集区域,[K+]0升高可能在癫痫样活动实际开始之前就已开始。癫痫样活动的特征可能会转变为反复强直放电发作状态或持续阵挛放电状态,类似于各种形式的癫痫持续状态。在这些状态中的任何一种情况下,尽管有明显的投射活动至齿状回,但我们都未观察到CA3区积极参与EC的癫痫样活动。即使应用了印防己毒素(20微摩尔),CA3区也未积极参与在内嗅皮质中产生的SLE。当将巴氯芬(2微摩尔)添加到含有印防己毒素的培养基中时,在内嗅皮质和CA3区均出现了SLE,这表明巴氯芬对抑制性中间神经元的抑制作用可以克服从内嗅皮质到海马的投射活动的“过滤”。