摘要
目的 :探讨慢性激活右侧胼胝体 (corpuscallosum ,CC)重建对侧尾壳核 (caudate putamen ,CPu) 海马 (hippocam pus,HPC)癫痫网络的跨半球机制。方法 :SD大鼠 5 0只。慢性强直电刺激 ( 6 0Hz,0 .4~ 0 .6mA ,2s)右侧CC(chronictetanizationoftherightCC ,CTRCC) ,一天一次 ,8d后再次施加强直电刺激 ,同步记录左侧CPu(LCPu)和左侧HPC(LHPC)电图。结果 : CTRCC①引起LCPu和LHPC出现深部电波的交互性抑制现象 ,LCPu电图出现持续尖波发放时交互抑制现象消失。②诱发LCPu和LHPC电图出现癫痫点燃现象。③未引起大鼠LCPu和LH PC电图点燃时 ,急性强直电刺激可诱发LCPu出现高幅失律 ,压抑LHPC具有频率特征的尖波连续发放。④联合运用慢性和急性强直电刺激可诱导LCPu或LHPC电图出现原发性后放。结论 :慢性激活RCC可促进对侧CPu HPC癫痫网络的重建 ,形成新的癫痫病灶。
Aim: To study the role of epileptic neural networks reestablished in contralateral caudate putamen (CPu)-hippocampus(HPC) by using chronic tetanization of the right corpus callosum (CTRCC). Methods: Experiments were performed on 50 SD rats under anaesthesia. The left CPu (LCPu) and the left HPC(LHPC) electrographs were synchronously recorded after acute tetanization following CTRCC (60 Hz, 0.4~0.6 mA, 2 s). Results: ①In contralateralization to the side implanted interconvertable network inhibition between the CPu and the HPC were induced by combinedly using chronic and acute tetanization of the RCC. ②Electrographic kindling in the LCPu or in the LHPC was recorded after CTRCC. ③In case the LCPu or the LHPC electrographs were not kindled after CTRCC, hypoarhythmia in the LCPu and reduced sharp waves in the HPC were induced by repetitive tetanization of the RCC once again. ④Primary afterdischarges in the LCPu or in the LHPC electrographs were evoked by combinedly using chronic and acute tetanization of the RCC. Conclusion: Pathophysiological neural networks in the CPu and in the HPC might be reestablished in another side of hemispheres by chronic over-activation of the right CC, which is related to epileptogenesis. Abnormal interactions between the two functional neural networks might be involved in formation of secondary epileptic focus.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2003年第2期165-169,共5页
Chinese Journal of Applied Physiology
基金
湖北省自然科学基金资助项目 ( 99J137)
关键词
大鼠
右侧胼胝体
尾壳核
海马
癫痫
电图
corpus callosum
caudate putamen
hippocampus
depth electrograph
epilepsy