The development of recurrent seizures after continuous intrahippocampal infusion of methionine sulfoximine in rats: a video-intracranial electroencephalographic study.
The development of recurrent seizures after continuous intrahippocampal infusion of methionine sulfoximine in rats: a video-intracranial electroencephalographic study.
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大鼠海马内连续输注甲硫氨酸亚砜亚胺后复发性癫痫发作的发展：一项视频颅内脑电图研究。
DOI：
10.1016/j.expneurol.2009.08.034
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发表时间：
2009
影响因子：
5.3
通讯作者：
Eid,Tore
中科院分区：
文献类型：
--
作者：
Wang,Yue;Zaveri,HittenP;Lee,Tih-ShihW;Eid,Tore
Glutamine synthetase is deficient in astrocytes in the epileptogenic hippocampus in human mesial temporal lobe epilepsy (MTLE). To explore the role of this deficiency in the pathophysiology of MTLE, rats were continuously infused with the glutamine synthetase inhibitor methionine sulfoximine (MSO, 0.625 μg/h) or 0.9% NaCl (saline control) unilaterally into the hippocampus. The seizures caused by MSO were assessed by video-intracranial electroencephalogram (EEG) monitoring. All (28 of 28) of the MSO-treated animals and none (0 of 12) of the saline-treated animals developed recurrent seizures. Most recurrent seizures appeared in clusters of 2 days' duration (median; range, 1 to 12 days). The first cluster was characterized by frequent, predominantly stage I seizures, which presented after the first 9.5 h of infusion (median; range, 5.5 to 31.7 h). Subsequent clusters of less-frequent, mainly partial seizures occurred after a clinically silent interval of 7.1 days (median; range, 1.8 to 16.2 days). The ictal intracranial EEGs shared several characteristics with recordings of partial seizures in humans, such as a distinct evolution of the amplitude and frequency of the EEG signal. The neuropathology caused by MSO had similarities to hippocampal sclerosis in 23.1% of cases, whereas 26.9% of the animals had minimal neuronal loss in the hippocampus. Moderate to severe diffuse neuronal loss was observed in 50% of the animals. In conclusion, the model of intrahippocampal MSO infusion replicates key features of human MTLE and may represent a useful tool for further studies of the cellular, molecular and electrophysiological mechanisms of this disorder.
