Burnham W M, Racine R J, Milgram N W, Albright P S
Department of Pharmacology, University of Toronto, Ontario, Canada.
Exp Neurol. 1989 Nov;106(2):150-5. doi: 10.1016/0014-4886(89)90088-5.
The kindling technique has been reported to produce a long-lasting enhancement in both the early and late phases of evoked potentials triggered from the kindled focus. It also alters paired-pulse facilitation and depression in the pathways which support these phenomena. The present experiment was designed to determine whether the drugs which antagonize secondary generalization in the kindling model also antagonize kindling-enhanced excitation in the pathways leading out of the focus. Multiple doses of phenytoin, carbamazepine, and clonazepam were therefore tested against single- and double-pulse evoked potentials triggered from the focus in rats that had been subjected to parital kindling from either the amygdala or the cortex. Responses were recorded in monosynaptic sites and in the mesencephalic reticular formation--a polysynaptic site thought to play an important role in secondary generalization. No drug-related effects were found on early evoked potential components, either in the single-pulse or the double-pulse paradigm. Kindling-enhanced late components ("late waves"), however, were clearly and selectively antagonized by clonazepam.
据报道，点燃技术可在由点燃灶触发的诱发电位的早期和晚期阶段产生持久增强。它还会改变支持这些现象的通路中的双脉冲易化和抑制。本实验旨在确定在点燃模型中拮抗继发性泛化的药物是否也能拮抗从点燃灶引出的通路中的点燃增强兴奋。因此，针对来自杏仁核或皮层进行部分点燃的大鼠，测试了多剂量的苯妥英钠、卡马西平和氯硝西泮对从点燃灶触发的单脉冲和双脉冲诱发电位的影响。在单突触部位和中脑网状结构（一个被认为在继发性泛化中起重要作用的多突触部位）记录反应。在单脉冲或双脉冲范式中，未发现药物对早期诱发电位成分有相关影响。然而，氯硝西泮能明显且选择性地拮抗点燃增强的晚期成分（“晚期波”）。
