Alterations of glial cell function in temporal lobe epilepsy
Alterations of glial cell function in temporal lobe epilepsy
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DOI：
10.1111/j.1528-1157.2000.tb01579.x
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发表时间：
2000-01-01
期刊：
影响因子：
5.6
通讯作者：
Lehmann, TN
中科院分区：
文献类型：
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作者：
Heinemann, U;Gabriel, S;Lehmann, TN
目的：比较癫痫和非癫痫海马细胞外K+调节。方法：用双管K+选择性参考微电极测量人和大鼠海马脑片CA1区的K+信号，通过重复肺泡刺激或离子导入诱导细胞外钾浓度增加，并通过钡阻断星形胶质细胞内的内向整流和背景K+通道。结果：在正常大鼠海马CAI锥体层，钡增加细胞外K+的积累诱导离子导入或逆向刺激以剂量依赖性的方式。同样，钡增强刺激诱导的K+信号从nonsclerosis campi（人类内侧颞叶癫痫），相反，钡未能做到这一点sclerosis campi（人类内侧颞叶癫痫，大鼠匹鲁卡品模型）。结论：我们的研究结果表明，在神经元密度降低（海马硬化）的地区，神经胶质细胞适应允许相当大的增加细胞外钾积累。这种增加可能涉及通过scenario区域的活动传输。
Purpose: Comparison of extracellular K+ regulation in sclerotic and nonsclerotic epileptic hippocampus.Methods: Measurements of K+ signals with double-barreled K+-selective reference microelectrodes in area CA1 of slices from human and rat hippocampus, induction of increases in extracellular potassium concentration by repetitive alvear stimulation or iontophoresis, and block of inward-rectifying and background K+ channels in astrocytes by barium.Results: In the CAI pyramidal layer from normal rat hippocampus, barium augmented extracellular K+ accumulation induced by iontophoresis or antidromic stimulation in a dose-dependent manner. Similarly, barium augmented stimulus-induced K+ signals from nonsclerotic hippocampi (human mesial temporal lobe epilepsy), in contrast, barium failed to do so in sclerotic hippocampi (human mesial temporal lobe epilepsy, rat pilocarpine model).Conclusions: Our findings suggest that in areas of reduced neuronal density (hippocampal sclerosis), glial cells adapt to permit rather large increases in extracellular potassium accumulation. Such increases might be involved in the transmission of activity through the sclerotic area.