Temporal profile of neuronal injury following pilocarpine or kainic acid-induced status epilepticus
Temporal profile of neuronal injury following pilocarpine or kainic acid-induced status epilepticus
复制标题
DOI：
10.1016/s0920-1211(99)00119-9
复制
发表时间：
2000-04-01
影响因子：
2.2
通讯作者：
Mello, LEAM
中科院分区：
文献类型：
--
作者：
Covolan, L;Mello, LEAM
毛果芸香碱和海人藻酸(KA)全身给药已被广泛用于建立大鼠颞叶癫痫模型。在这里，我们比较了两种模型中选择性易损神经元的区域分布和癫痫持续状态(SE)后神经元损伤的时间演变。采用Galyas银染技术，对53个不同脑区的嗜银神经元进行了0-3(最小-最小)的测量。海人藻酸诱导SE后2.5h，仅有少量神经元呈银染，而匹罗卡品组大鼠大脑皮层、海马、杏仁核和下丘脑结构中可见大量银染细胞。一般而言，SE开始和灌流时间之间的8或24小时间隔产生了最强烈的神经元银染。在大脑皮层、海马区，匹罗卡品诱导的神经元银染明显高于红藻氨酸处理。梨状内核、杏仁复合体和下丘脑。另一方面，在丘脑、部分皮质、屏蔽区、外侧隔区和尾壳核，红藻氨酸诱导的神经元银染也较明显，但出现的时间晚于匹罗卡品处理的动物。在两种SE模型中，神经元损伤在几乎相同的脑区被发现，但强度和时程曲线不同。有人建议，在寻找神经保护剂时，应该考虑到细胞损伤时间分布的这种差异。(C)2000 Elsevier Science B.V.保留所有权利。
Systemic administration of pilocarpine and kainic acid (KA) has been extensively used to model temporal lobe epilepsy in rats. Here the regional distribution of selectively vulnerable neurons and the temporal evolution of such neuronal injury after status epilepticus (SE) are compared in both models. Using the silver staining technique of Gallyas, argyrophilic neurons were measured on a 0-3 (least-most) scale in 53 different brain areas. Few neurons were silver-stained 2.5 h after kainate-induced SE, but many silver-stained cells could be seen in most neocortical, hippocampal, amygdaloid and hypothalamic structures for pilocarpine group. In general, 8 or 24 h intervals between SE onset and perfusion times yielded the most intense neuronal silver-impregnation. Pilocarpine-induced neuronal silver impregnation was more prominent than that induced by kainate treatment for many areas in cortex, hippocampus. endopiriform nucleus, amygdaloid complex and hypothalamus. On the other hand, in the thalamus, some cortical areas, claustrum, lateral septum and caudoputamen, kainate-induced neuronal silver staining was also prominent, but occurred later than in pilocarpine-treated animals. Neuronal injury was found in almost the same brain areas in both models of SE but with different intensity levels and time course profiles. It was suggested that such differences in the temporal profile of cell damage should be taken into account when searching for neuroprotective agents. (C) 2000 Elsevier Science B.V. All rights reserved.