【作者】 刁芳明；

【导师】 韩丹；

【作者基本信息】 武汉大学 ， 生理学， 2004， 硕士

【摘要】 本工作目的在于探讨强直电刺激大鼠右侧尾壳核(caudate putamen，CPu)重建双侧海马(hippocampus，HPC)癫痫电网络的细胞电生理机制。实验共用雄性SD大鼠101只，体重200～250g。急性强直电刺激(60Hz，2s，0.4～0.6mA)右侧尾壳核(acute tetanization of the right caudate putamen，ATRC)或右背海马(acute tetanization of the right dorsal hippocampus，ATRDH)，同步记录双侧前背HPC神经元单位放电，ATRC同步记录双侧HPC深部电图。比较激活右侧CPu到达双侧HPC或者激活右侧HPC到达双侧HPC时，经历了不同的神经通路长度对HPC癫痫电网络重建过程的影响，以及单个神经元电活动信息编码特征。结果表明：(1)ATRC可以促使HPC癫痫电网络的形成，显现出双侧HPC同步化的癫痫电活动；(2)ATRC和ATRDH均能明显调制单个HPC神经元的紧张式放电成为节律性爆发式放电；ATRC引起的HPC爆发式单位放电每串持续时间即串长(650.738±56.419ms，n=120)长、爆发式放电间期(interbursting interval，IBI，772.600±46.665ms，n=90)短；相反，ATRDH引起HPC的爆发式单位放电特征是串长短(270.612±19.917 ms，n=123)(T=6.353，P＜0.001)、IBI长(1373.663±121.236ms，n=103)(T=4.627，P＜0.001)；(3)ATRC诱发的HPC细胞单位后放电时程长(7.06±0.776s，n=104)、潜伏期也长(8.77±1.231trains，n=30)，而ATRDH诱发的单位后放电时程短(3.93±0.657s，n=33)(T=0.3079，P＜0.001)、潜伏期也短(3.33±0.681trains，n=15)T=3.681，P＜0.001)；(4)ATRC可诱导HPC爆发式单位放电和单位后放电之间的直接转换；(5)ATRC可促进双侧HPC神经元单位电活动的同步化或交互性作用。结果证实：激活CPu-HPC长路径神经通路可导致双侧HPC神经元长时程癫痫相关性电活动的形成，促进HPC癫痫电网络的重建，引发双侧颞叶癫痫的发作。激活右侧CPu，HPC神经元信息编码特征是爆发式单位放电的串长较长，IBI较短，具有神经元癫痫相关性电活动的放大作用；而激活右侧HPC后，HPC神经元信息编码特征是爆发式单位放电串长短，IBI较长，即激活到HPC不同的神经元通路，HPC神经元信息编码特征不同。很可能，激活了的CPu-HPC通路在HPC癫痫电网络病理性神经信息传递中可能起着重要的生物放大器作用。更多还原

【Abstract】 The purpose was to study the cellular electrophisiological mechanism of epileptic networks in dual hippocampi reestablished by overactivation of the right caudate putamen (CPu). The experiments were performed on 101 male Sprague Dawley rats weighting 200~250g. Acute tetanization (60Hz, 2s, 0.4~0.6mA) of the right caudate putamen (ATRC) or of the right dorsal hippocampus (ATRDH) was 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 those of the ATRDH, bilateral hippocampal depth electrograhgh were also simultaneously recorded after the ATRC. Neuronal epilepsy-related firing patterns were analyzed according to activated neural pathway length from the RCPu to the dual hippocampi, or from the right dorsal HPC to ipsilateral hippocampal local networks and contralateral HPC. Results demonstrated that: (1) ATRC could facilitate the formation of hippocampal epileptic networks, and presented the synchronaztion of epilepsy related electric activities in bilateral hippcampi. (2) The firing pattern of single hippocampal neuron was obviously modulated both by the ATRC and by the ATPDH. There were long duration bursting (650.738?6.419 ms, n=120) with short interbursting interval (IBI)(772.600 +46.665ms, n=90) of single neuron induced by the ATRC, while short duration bursting (270.612 + 19.917 ms, n=123) (T=6.353, P<0.001)of single neuron with long IBI(1373.663 ?121.236ms, n=103) (T=4.627, P<0.001)by the ATPDH. (3) There were long duration single unit afterdischarges (7.06 +0.776s, n=104) with long latency (8.77 + 1.231trains, n=30) induced by the ATRC, while short duration single unit afterdischarges(3.93 + 0.657S, n=33)( T=0.3079, P<0.001)with short latency (3.33+ 0.681trains, n=15) (7=3.681, P0.001) induced by the ATPDH. (4) ATRC could induce the immediate transition between single unit bursting and afterdischarges. (5) Pairs of cellular electric activities in bilateral hippocampi were synchronouse or interactive inhibiting after repeated administration of the ATRC. The results suggest that long duration single unit bursting or afterdischarges in bilateral hippocampi could be brought about by overactivation oflong-distance neural pathway from the right CPu to the dual hippocampi, which might be an important cellular mechanism of hippocampal epileptic networks reconstruction. From these phenomina the following conclusion can be drawn that there was different information encoding charisteristic when different neural pathway was activated. The activated CPu-HPC functional neural pathway might act as the amplifier of the signal of epilepsy-related activities of single neuron in bilateral hippocampi.更多还原