红藻酸致大鼠癫痫模型短潜伏期体感诱发电位分析  

Analysis on Short Latency Somatosensory Evoked Potentials in Convulsive Rats Induced by Kainic Acid

作　　者：罗晓红[1] 韩筱玉[1] 王晓姝[1] 何阳[1] 

机构地区：[1]兰州军区兰州总医院神经内科

出　　处：《西北国防医学杂志》1998年第1期14-16,共3页Medical Journal of National Defending Forces in Northwest China

摘　　要：目的：了解癫痫发作时大脑神经元的功能状态。方法：２０只红藻酸致痫大鼠于癫痫发作前、急性发作期、慢性发作期经正中神经刺激对短潜伏期体感诱发电位（ＳＬＳＥＰ）进行测定。结果：大鼠ＳＬＳＥＰ波形为一小的Ｎ１波后接一大的Ｐ１波；癫痫急性发作期改变为Ｎ１、Ｐ１波的ＰＬ延长，波幅降低，有３例波形缺失；慢性发作期仅Ｐ１波的Ｐ１较前缩短。结论：癫痫急性发作期Ｎ１、Ｐ１波的改变与兴奋性氨基酸的神经元毒性作用及继发性缺血、缺氧致神经元损伤有关。慢性发作期Ｐ１波缩短的机理有待进一步研究。Purpose:To explore the functional state of cortex neurons during convulsive state.Methods:The short latency somatosensory evoked potentials(SLSEPs)of 20 convulsive rats induced by kainic acid were detected through electric stimulation on forepaw(median nerve)during preconvulsion,acute attack period and chronic epileptic period.Results:The waveform of rats′SLSEPs was a small N1 followed by a large P1(N1P1).During acute attack period,there was significantly prolonged PL and markedly reduced amplitudes of N1 and P1,and 3 rats had wave deficits.In chronic epileptic period,only PL of P1 shortened than preconvulsion.Conclusion:The changes of N1P1 in acute attack period are related with the neuron toxic action of excitatory amino acids and lesions made by secondary ischemia and hypoxia.The P1 change in chronic epileptic period remains to be further studied.

关 键 词：动物实验 鼠 癫痫 红藻酸 短潜伏期体感诱发电位 

分 类 号：Q95-33[生物学—动物学]