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目的匹鲁卡品(pilocarpine)癫痫模型的潜伏期被认为是其癫痫自发的形成过程。本实验采用小鼠匹鲁卡品模型,研究潜伏期内电刺激诱导的后放电阈值(ADT)以及脑电(EEG)频谱能量的变化。方法 ICR小鼠立体定位在右侧海马CA3区并进行电极植入手术。休息7 d后用恒流电刺激器(刺激参数为单向方波,60 Hz,波宽为1 ms,刺激时间为1 s)测定基础后放电阈值和记录正常状态下EEG基线。腹腔注射匹鲁卡品(200 mg·kg-1)诱导持续癫痫发作(SE),60 min SE后地西泮(1 mg·kg-1)终止。在SE后第5,10,15,20天测定CA3区后放电阈值。动物每天白天记录12 hEEG以观察自发发作从而判断潜伏期是否结束。结果在潜伏期内,后放电阈值相对于SE前明显抬高,潜伏期后明显回落。同时,在潜伏期EEG的delta节律相对能量升高而theta节律相对能量降低。进一步相关性分析发现,癫痫阈值的抬高与Delta节律能量增加存在着明显的正相关,与theta节律的降低存在着明显的负相关。结论匹鲁卡品模型潜伏期的可能与海马后放电阈值的过度抬高以及相应EEG频谱能量的变化有关,delta和theta节律在癫痫形成过程中的作用值得进一步关注。
Purpose The incubation period of the pilocarpine epilepsy model is considered as the spontaneous formation of epilepsy. In this study, the mouse pilocarpine model was used to study the changes of post-discharge threshold (ADT) and EEG energy spectrum induced by electrical stimulation during the incubation period. Methods ICR mice were stereotaxically located in the right hippocampal CA3 region and underwent electrode implantation. Rest 7 d after the constant current stimulation (stimulus parameters for the one-way square wave, 60 Hz, wave width of 1 ms, stimulation time of 1 s) after the baseline discharge threshold and record under normal EEG baseline. Intraperitoneal injection of pilocarpine (200 mg · kg -1) induced a sustained seizure (SE), and diazepam (1 mg · kg -1) terminated after 60 min of SE. The discharge threshold of CA3 area was measured on the 5th, 10th, 15th and 20th days after SE. Animals were recorded daily for 12 hEEG to observe spontaneous seizures to determine whether the incubation period was over. Results During the incubation period, the post-discharge threshold was significantly higher than that before SE, and then decreased significantly after the incubation period. At the same time, the relative energy of the delta rhythm of EEG increased during the incubation period while the relative energy of theta rhythm decreased. Further correlation analysis showed that there was a significant positive correlation between elevation of the epilepsy threshold and increase of Delta rhythm energy and a significant negative correlation with theta rhythm reduction. Conclusion The possible inducement of pilocarpine model may be related to the excessive increase of hippocampal post-discharge threshold and the change of EEG spectral energy. The role of delta and theta rhythms in epilepsy deserves further attention.