Schmitz D, Zhang C L, Chatterjee S S, Heinemann U
Institut für neurophisiologie Zentrum für Physiologie und Pathophysiologie Universität zu Köln, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1995 Apr;351(4):348-55. doi: 10.1007/BF00169074.
Methysticin is one of the constituents of Piper methysticum which possesses anticonvulsant and neuroprotective properties. Its effects on different in vitro seizure models were tested using extracellular recordings in rat temporal cortex slices containing the hippocampus and the entorhinal cortex. Elevating [K+]0 induced seizure-like events with tonic and clonic electrographic phases in area CA1. Lowering [Ca2+]0 caused recurrent seizure like episodes with large negative field potential shifts. Lowering Mg2+ induced short recurrent discharges in area CA3 and CA1 while ictaform events lasting for many seconds were induced in the subiculum, entorhinal and temporal neocortex. In the hippocampus the activity stayed stable over a number of hours. In contrast, the ictaform events in the subiculum, entorhinal and temporal cortex changed their characteristics after one to two hours to late recurrent discharges. In a concentration-range from 10 to 100 microM methysticin reversibly blocked all these types of epileptiform activity. Decreases in [Ca2+]0 and associated slow field potentials evoked by repetitive stimulation of the stratum radiatum or the alveus remained almost unaffected by methysticin. A paired pulse stimulus paradigm used to test for effects of methysticin on synaptically evoked transient field potentials in normal medium revealed interference with mechanisms involved in frequency potentiation. While responses to alvear stimulation were largely unaffected, the responses to a paired pulse stimulus to stratum radiatum were depressed over the whole range of tested stimulus intervals. The findings suggest that methysticin has effects on different patterns of epileptiform activity possibly by interfering with processes responsible for frequency potentiation.
紫锥菊素是卡瓦胡椒的成分之一，具有抗惊厥和神经保护特性。利用包含海马体和内嗅皮质的大鼠颞叶皮质切片的细胞外记录，测试了其对不同体外癫痫模型的作用。升高[K⁺]₀在CA1区诱发了具有强直和阵挛性电图阶段的癫痫样事件。降低[Ca²⁺]₀导致复发性癫痫样发作，并伴有大的负向场电位变化。降低Mg²⁺在CA3区和CA1区诱发短暂的复发性放电，而在海马下托、内嗅皮质和颞叶新皮质诱发持续数秒的癫痫样事件。在海马体中，活动在数小时内保持稳定。相比之下，海马下托、内嗅皮质和颞叶皮质中的癫痫样事件在一到两小时后其特征转变为晚期复发性放电。在10至100微摩尔的浓度范围内，紫锥菊素可逆转性阻断所有这些类型的癫痫样活动。降低[Ca²⁺]₀以及重复刺激辐射层或齿状回所诱发的相关慢场电位几乎不受紫锥菊素的影响。在正常培养基中使用配对脉冲刺激范式来测试紫锥菊素对突触诱发的瞬态场电位的影响，结果显示其对频率增强所涉及的机制有干扰作用。虽然对齿状回刺激的反应基本未受影响，但在整个测试刺激间隔范围内，对辐射层配对脉冲刺激的反应均受到抑制。这些发现表明，紫锥菊素可能通过干扰负责频率增强的过程，对不同模式的癫痫样活动产生影响。
