Sasaki S, Warita H, Abe K, Komori T, Iwata M
Department of Neurology, Neurological Institute, Tokyo Women's Medical College, Japan.
Neuroreport. 2001 May 25;12(7):1359-62. doi: 10.1097/00001756-200105250-00014.
Immunocytochemical and quantitative analyses were used to correlate the localisation of excitatory amino acid transporter proteins EAAT1, EAAT2 with time in spinal motoneurones of presymptomatic and symptomatic mice with the G93A mutant SOD1 gene. Specimens from age-matched non-transgenic wild-type mice served as controls. EAAT1 and EAAT2 immunoreactivity was well-preserved in the gray matter in both controls and transgenic mice at all ages, and there was no difference in the expression of EAAT1 and EAAT2 immunoreactivity between controls and transgenic mice. These findings suggest that EAAT1 and EAAT2 may not play a pivotal role in the degeneration of motoneurons in this animal model.
采用免疫细胞化学和定量分析方法，将携带G93A突变型SOD1基因的症状前和有症状小鼠脊髓运动神经元中兴奋性氨基酸转运蛋白EAAT1、EAAT2的定位与时间进行关联。来自年龄匹配的非转基因野生型小鼠的标本用作对照。在所有年龄段的对照小鼠和转基因小鼠中，EAAT1和EAAT2免疫反应性在灰质中均保存良好，对照小鼠和转基因小鼠之间EAAT1和EAAT2免疫反应性的表达没有差异。这些发现表明，在该动物模型中，EAAT1和EAAT2可能在运动神经元变性中不发挥关键作用。
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