Mechanisms in the development of limbic status epilepticus and hippocampal neuron loss: an experimental study in a model of status epilepticus induced by kindling-like electrical stimulation of the deep prepyriform cortex in rats.
Mechanisms in the development of limbic status epilepticus and hippocampal neuron loss: an experimental study in a model of status epilepticus induced by kindling-like electrical stimulation of the deep prepyriform cortex in rats.
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边缘系统癫痫持续状态和海马神经元丢失的发生机制：大鼠前梨状皮层深部引火样电刺激诱发癫痫持续状态模型的实验研究。
DOI：
10.18926/amo/32652
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发表时间：
1992
影响因子：
0.5
通讯作者：
S. Otsuki
中科院分区：
文献类型：
--
作者：
Koutarou Inoue;K. Morimoto;Keiko Sato;N. Yamada;S. Otsuki
本文建立了一种在清醒大鼠大脑皮层深层以20 Hz、每分钟20秒、持续180分钟的间歇性电刺激诱导癫痫持续状态的新模型。无药组16只大鼠中有9只发生SE。在该状态亚组中，诱导SE所需的刺激序列数为125.6 +/- 12.7（平均+/- SEM），刺激结束后发生的自我持续癫痫发作活动（SSSA）的平均持续时间为295.4 +/- 111.4分钟。部分动物出现继发性全身性癫痫发作。与假手术组相比，状态亚组海马CA3锥体细胞层与刺激部位同侧及双侧CA1区细胞明显减少。此外，刺激后SSSA持续时间与状态亚组双侧CA1和同侧CA3亚区完整锥体神经元总数呈显著负相关。在刺激过程中，状态亚组和非状态亚组在放电后（ADs）次数和总AD持续时间方面存在显著差异。苯巴比妥预处理（30 mg/kg）完全阻止SE的发生和海马细胞的损失。用非竞争性n-甲基- d -天冬氨酸（NMDA）受体拮抗剂MK-801（0.25或1 mg/kg）预处理也可以防止海马细胞损失，尽管它不能完全阻断SE的产生，这表明SE发展和海马损伤的机制分离。这些结果表明，长时间SSSA确实会导致海马损伤，并且严重依赖于NMDA受体的参与。
A new model of status epilepticus (SE), which was induced by intermittent electrical stimulation (20 Hz for 20 sec every min for 180 min) of the deep prepyriform cortex, has been developed in the conscious rat. SE was induced in 9 of 16 rats in the drug-free group. The number of stimulation trains required to induce SE in this status subgroup was 125.6 +/- 12.7 (mean +/- SEM) and the mean duration of self-sustained seizure activity (SSSA) occurring after cessation of the stimulation session was 295.4 +/- 111.4 min. Some animals showed secondary generalized seizures. Significant cell loss was observed in the hippocampal CA3 pyramidal cell layer ipsilateral to the stimulation site and bilateral CA1 areas in the status subgroup compared with the group subjected to sham operation. In addition, there was a significant negative correlation between the duration of SSSA subsequent to the stimulation session and the total number of intact pyramidal neurons observed in the bilateral CA1 and ipsilateral CA3 subfields of the status subgroup. There were significant differences between the status and non-status subgroups with respect to the number of afterdischarges (ADs) and the total AD duration during the stimulation session. Pretreatment with phenobarbital (30 mg/kg) prevented the development of SE and hippocampal cell loss completely. Pretreatment with MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist (0.25 or 1 mg/kg), also prevented hippocampal cell loss, although it did not block SE generation completely, which suggests dissociation of the mechanisms underlying the development of SE and hippocampal damage. These results indicate that prolonged SSSA actually causes hippocampal damage and it is critically dependent upon NMDA receptor participation.