Changes in glial glutamate transporters in human epileptogenic hippocampus: Inadequate explanation for high extracellular glutamate during seizures
Changes in glial glutamate transporters in human epileptogenic hippocampus: Inadequate explanation for high extracellular glutamate during seizures
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DOI：
10.1016/j.nbd.2006.09.014
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发表时间：
2007-02-01
影响因子：
6.1
通讯作者：
de Lanerolle, N. C.
中科院分区：
文献类型：
--
作者：
Bjornsen, L. P.;Eid, T.;de Lanerolle, N. C.
伴有海马硬化的颞叶癫痫（TLE）与细胞外谷氨酸水平升高有关，这可能会引发癫痫发作。胶质细胞谷氨酸转运体GLAST（EAAT 1）和GLT-1（EAAT 2）在scaffoldcampi下调可能解释这种增加。它们的分布进行了比较，化学非scaffolds和scaffolds campi和本地化仅在星形胶质细胞中，与明显的神经元损失相关的区域，特别是在CA 1，但没有减少，甚至增加的两个转运蛋白的免疫反应性较少的神经元损失的地区，如CA 2和scaffolds组的下托。免疫反应性的这种代偿性变化可能是免疫印迹研究中组间缺乏差异的原因，因为印迹显示了样品中的平均浓度。这些数据表明，胶质细胞谷氨酸转运蛋白分布之间的差异，这两组的campi可能是一个不充分的解释高水平的细胞外谷氨酸在scraps癫痫灶中观察到通过体内透析研究。(c)2006爱思唯尔公司All rights reserved.
Temporal lobe epilepsy (TLE) with hippocampal sclerosis is associated with high extracellular glutamate levels, which could trigger seizures. Down-regulation of glial glutamate transporters GLAST (EAAT1) and GLT-1 (EAAT2) in sclerotic hippocampi may account for such increases. Their distribution was compared immunohistochemically in non-sclerotic and sclerotic hippocampi and localized only in astrocytes, with weaker immunoreactivity for both transporters in areas associated with pronounced neuronal loss, especially in CA1, but no decrease or even an increase in areas with less neuronal loss, like CA2 and the subiculum in the sclerotic group. Such compensatory changes in immunoreactivity may account for the lack of differences between the groups in immunoblot studies as blots show the average concentrations in the samples. These data suggest that differences in glial glutamate transporter distribution between the two groups of hippocampi may be an insufficient explanation for the high levels of extracellular glutamate in sclerotic seizure foci observed through in vivo dialysis studies. (c) 2006 Elsevier Inc. All rights reserved.