Epilepsy induced by extended amygdala-kindling in rats:: lack of clear association between development of spontaneous seizures and neuronal damage
Epilepsy induced by extended amygdala-kindling in rats:: lack of clear association between development of spontaneous seizures and neuronal damage
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DOI：
10.1016/j.eplepsyres.2004.08.008
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发表时间：
2004-12-01
影响因子：
2.2
通讯作者：
Löscher, W
中科院分区：
文献类型：
--
作者：
Brandt, C;Ebert, U;Löscher, W
颞叶癫痫（TLE）是最常见的癫痫类型，大多数患者在边缘脑区域（包括海马、杏仁核和海马旁区域）显示出明显的神经元损失。颞叶癫痫患者海马损害的特点是广泛的神经元损失在CA 3和CA 1部门和门的齿状回。关于这种海马损伤（称为海马硬化）是TLE的原因还是结果，存在长期且持续的争论。此外，海马损伤可能有助于TLE的进展特征。本研究旨在确定大鼠杏仁核延长点燃后自发性复发性癫痫发作（SRS）的发生是否与神经元损伤有关。选择TLE的点燃模型是因为先前的研究表明，只有部分大鼠在延长点燃后发生SRS，因此可以比较接受相同数量杏仁核刺激但发生或未发生SRS的大鼠的脑病理学。对于延长点燃，每周3-5天每天刺激大鼠两次，最多约280次刺激。在长期EEG/视频监测期间，在延长点燃期间在50%的大鼠中观察到SRS。SRS常以肌阵挛性抽搐或局灶性发作开始，随后发展为继发性全身性发作，因此SRS的发展再现了诱发性发作的早期点燃。海马CA 1、CA 3区、杏仁核、海马旁区及丘脑未见明显神经元变性。延长点燃后，齿状门神经元密度的显著双侧减少，但这种门细胞密度的减少在有和没有观察到SRS的大鼠之间没有显著差异。肺门神经元总数和肺门体积的测定表明，齿状门神经元密度的降低是由于肺门面积的扩大，而不是神经元损伤。数据表明，延长点燃不会导致任何海马损伤类似海马硬化，但SRS的发展，在没有这样的损害。(C)2004 Elsevier B. V.保留所有权利。
Most patients with temporal lobe epilepsy (TLE), the most common type of epilepsy, show pronounced loss of neurons in limbic brain regions, including the hippocampus, amygdala, and parahippocampal regions. Hippocampal damage in patients with TLE is characterized by extensive neuronal loss in the CA3 and CA1 sectors and the hilus of the dentate gyrus. There is a long and ongoing debate on whether this type of hippocampal damage, referred to as hippocampal sclerosis, is the cause or consequence of TLE. Furthermore, hippocampal damage may contribute to the progressive features of TLE. The present study was designed to determine whether development of spontaneous recurrent seizures (SRS) after extended kindling of the amygdala in rats is associated with neuronal damage. The kindling model of TLE was chosen because previous studies have shown that only part of the rats develop SRS after extended kindling, thus allowing to compare the brain pathology of rats that received the same number of amygdala stimulation but did or did not develop SRS. For extended kindling, rats were stimulated twice daily 3-5 days a week for up to about 280 stimulations. During long-term EEG/video monitoring, SRS were observed in 50% of the rats over the period of extended kindling. SRS often started with myoclonic jerks or focal seizures and subsequently progressed into secondarily generalized seizures, so that the development of SRS recapitulated the earlier kindling of elicited seizures. No obvious neurodegeneration was observed in the CA1 and CA3 sectors of the hippocampus, the amygdala, parahippocampal regions or thalamus. A significant bilateral reduction in neuronal density was determined in the dentate hilus after extended kindling, but this reduction in hilar cell density did not significantly differ between rats with and without observed SRS. Determination of the total number of hilar neurons and of hilar volume indicated that the reduced neuronal density in the dentate hilus was due to expansion of hilar area but not to neuronal damage. The data demonstrate that extended kindling does not cause any hippocampal damage resembling hippocampal sclerosis, but that SRS develop in the absence of such damage. (C) 2004 Elsevier B.V. All rights reserved.