Zhang Jin, Ding Mei-ping, Liu Zhao, Xiao Bo, Li Guo-liang, Zhou Fu-you
Department of Neurology, Second Affilited Hosptial, Zhejiang University College of Medicine, Hangzhou 310009, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 May;23(2):200-3.
To observe the intracellular calcium ion spatio-temporal and dynamic changes in the hippocampal neuronal culture model of epilepsy induced by low magnesium ion medium, and to explore the relationship between calcium ion and epilepsy.
Applying both laser scanning confocal microscope and patch clamp to timely observe the changes of [Ca2+]i and electrophysiological in the hippocampal neuronal culture model of epilepsy, and the influence of NMDA receptor-gated channels retarder and non-NMDA receptor-gated channels retarder.
After the hippocampal nerve cell broken into epileptiform discharges, [(Ca2+]i rapidly ascended to (620 +/- 70) nmol/L, NMIDA acceptor retarder (MK-801, 10 micromol/L) and non-NMDA acceptor retarder (NBQX, 10 micromol/L) reduced [Ca2+]i ascendance. Recovery of the elevated [Ca2+]i was obviously delay, after 90 min and 150 min epileptiform discharges, it took (114.8 +/- 5.2) min and (135.0 +/- 22.7) min (P < 0.05) respectively.
In vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons
观察低镁离子培养基诱导的癫痫海马神经元培养模型中细胞内钙离子的时空及动态变化,探讨钙离子与癫痫的关系。
应用激光扫描共聚焦显微镜和膜片钳技术,及时观察癫痫海马神经元培养模型中细胞内钙离子浓度([Ca2+]i)变化及电生理情况,以及N-甲基-D-天冬氨酸(NMDA)受体门控通道阻滞剂和非NMDA受体门控通道阻滞剂的影响。
海马神经细胞爆发癫痫样放电后,[Ca2+]i迅速上升至(620±70)nmol/L,NMDA受体阻滞剂(MK-801,10μmol/L)和非NMDA受体阻滞剂(NBQX,10μmol/L)可降低[Ca2+]i的上升幅度。癫痫样放电90分钟和150分钟后,升高的[Ca2+]i恢复明显延迟,分别需要(114.8±5.2)分钟和(135.0±22.7)分钟(P<0.05)。
体外癫痫持续状态可导致海马神经元细胞内钙水平持续升高