Turski W A, Cavalheiro E A, Ikonomidou C, Mello L E, Bortolotto Z A, Turski L
Brain Res. 1985 Dec 30;361(1-2):309-23. doi: 10.1016/0006-8993(85)91302-2.
The effects of 2-chloroadenosine, aminophylline, bicuculline, beta-carboline-3-carboxylic acid methylester and Ro 15-1788 on seizures produced by pilocarpine were examined in rats. In animals pretreated with aminophylline at doses of 25-100 mg/kg, non-convulsant dose of pilocarpine, 100 mg/kg, resulted in severe motor limbic seizures, which rapidly developed into the status epilepticus. Electroencephalographic monitoring showed progressive evolution of seizure activity with initial high-voltage fast activity followed by high-voltage spiking and electrographic seizures. Morphological analysis of frontal forebrain sections with light microscopy demonstrated widespread damage to the hippocampal formation, thalamus, amygdala, olfactory cortex, substantia nigra and neocortex. Bicuculline, 2 mg/kg, beta-carboline-3-carboxylic acid methylester, 5 mg/kg, and Ro 15-1788, 50 mg/kg, did not augment seizures produced by pilocarpine, 100 mg/kg. 2-Chloroadenosine, 5 and 10 mg/kg, blocked the appearance of behavioral and electrographic seizures produced by pilocarpine, 380 mg/kg, and prevented the occurrence of brain damage. The results indicate that purinergic mechanisms are involved in the buildup of pilocarpine-induced convulsions and seizure-related brain damage in rats.
在大鼠中研究了2-氯腺苷、氨茶碱、荷包牡丹碱、β-咔啉-3-羧酸甲酯和Ro 15-1788对毛果芸香碱诱发癫痫发作的影响。在用25-100mg/kg剂量的氨茶碱预处理的动物中，100mg/kg的非惊厥剂量毛果芸香碱会导致严重的肢体边缘运动性癫痫发作，并迅速发展为癫痫持续状态。脑电图监测显示癫痫活动逐渐演变，最初为高电压快速活动，随后是高电压棘波和脑电图癫痫发作。用光镜对额叶前脑切片进行形态学分析，结果显示海马结构、丘脑、杏仁核、嗅觉皮质、黑质和新皮质广泛受损。2mg/kg的荷包牡丹碱、5mg/kg的β-咔啉-3-羧酸甲酯和50mg/kg的Ro 15-1788不会增强100mg/kg毛果芸香碱诱发的癫痫发作。5mg/kg和10mg/kg的2-氯腺苷可阻断380mg/kg毛果芸香碱诱发的行为性和脑电图癫痫发作的出现，并预防脑损伤的发生。结果表明，嘌呤能机制参与了大鼠毛果芸香碱诱发惊厥和癫痫相关脑损伤的形成过程。
