激活大鼠右侧尾壳核重建双侧海马癫痫网络的细胞机制(英文)  

Cellular mechanism of epileptic networks in dual hippocampi reestablished by tetanization of the right caudate putamen in rats

作　　者：刁芳明[1] 韩丹[1] 尹世金[2] 甘丽[1] 邹祖玉[3] 

机构地区：[1]武汉大学医学院生理学系,湖北武汉430071 [2]中南民族大学生物医学工程研究所,湖北武汉430074 [3]武汉大学医学院病理学与病理生理学系,湖北武汉430071

出　　处：《中国神经科学杂志》2004年第1期1-8,共8页

基　　金：湖北省自然科学基金资助项目 (2 0 0 3ABA12 3 )

摘　　要：目的　 探讨强直电刺激大鼠右侧尾壳核 (rightcaudateputamen ,RCPu)重建双侧海马 (hippocampus,HPC)癫痫电网络的细胞机制。 方法　 实验共用雄性SD大鼠 10 1只 ,体重 2 0 0～ 2 5 0g。急性强直电刺激 (6 0Hz ,2s,0 .4～ 0 .6mA)RCPu (acutetetanizationoftherightcaudateputamen ,ATRC)或右背HPC(acutetetanizationoftherightdorsalhippocampus,ATRDH) ,同步记录双侧前背HPC神经元单位放电 ,比较激活RCPu或RHPC时 ,神经通路长度对HPC癫痫电网络重建过程中单个神经元电活动的影响。 结果　(1)ATRC和ATRDH均能明显地调制单个HPC神经元的紧张式放电成为节律性爆发式放电。 (2 )ATRC引起的HPC爆发式单位放电串放电时程长[(6 5 0 .738± 5 6 .4 19)ms ,n =12 0 ]、串间隔短 [(interburstinginterval,IBI ,(772 .6 0 0± 4 6 .6 6 5 )ms,n =90 ) ;相反 ,ATRDH引起HPC的爆发式单位放电特征是串放电时程短 [(2 70 .6 12± 19.917)ms,n =12 3](T =6 .35 3,P <0 .0 0 1)、IBI长 [(1373.6 6 3± 12 1.2 36 )ms,n =10 3](T =4 .6 2 7P <0 .0 0 1)。 (3)ATRC诱发的海马细胞单位后放电时程长 [(7.0 6± 0 .776 )s,n =10 4 ]、潜伏期长 [(8.77± 1.2 31)trains ,n =30 ],而ATRDH诱发的单位后放电时程短 [(3.93± 0 .Objective To study the cellular mechanism of epileptic networks in dual hippocampi reestablished by overactivation of the right caudate putamen (RCPu). Methods The experiments were performed on 101 male Sprague Dawley rats weighting 200-250 g. Acute tetanization (60 Hz, 2 s, 0.4-0.6 mA) of the right caudate putamen (ATRC) or of the right dorsal hippocampus (ATRDH) were administrated to establish rat epilepsy model. A pair of single unit recordings from bilateral hippocampi was simultaneously used to detect the effects of the ATRC or the ATRDH. Neuronal epilepsy-related firing patterns were analyzed according to activated neural pathway length from the CPu to the dual hippocampi, or from the anterior dorsal HPC to ipsilateral local networks and contralateral HPC. Results (1) The firing pattern of single hippocampal neuron was obviously modulated by the ATRC or by the ATRDH. (2) There were long duration bursting \[(650.738±56.419) ms, n=120\] with short interbursting interval (IBI) \[(772.600±46.665)ms, n=90\] of single neurons induced by the ATRC, while short duration bursting \[(270.612±19.917)ms, n=123\] (T=6.353,P< 0.001 )of single neurons with long IBI \[(1373.663±121.236)ms, n=103\] ( T=4.627, P<0.001) by the ATRDH. (3) There were long duration single unit afterdischarges[(7.06±0.776) s, n=104] with long latency[(8.77±1.231)trains, n=30] induced by the ATRC, while short duration single unit afterdischarges \[(3.93±0.657)s,n=33\] ( T=0.3079,P<0.001)with short latency \[(3.33±0.681)trains,n=15\] (T=3.681,P<0.001) by the ATRDH. (4) Pairs of cell unit discharges or of electrographic kindling in bilateral hippocampi might be partially or completely synchronized by the ATRC. Conclusion It was clarified that long duration bursting or single unit afterdischarges in bilateral hippocampi could be brought about by overactivation of long-distance neural pathway from the RCPu to the dual hippocampi, which might be an important cellular mechanism of the HPC epileptic network reconstruction. The activated CPu-HPC f

关 键 词：大鼠 右侧尾壳核 双侧海马 癫痫 细胞机制 强直电刺激 

分 类 号：R742.1[医药卫生—神经病学与精神病学] R-33[医药卫生—临床医学]