Tardive decrease of astrocytic glutamate transporter protein in transgenic mice with ALS-linked mutant SOD1

被引:21
|
作者
Warita, H [1 ]
Manabe, Y [1 ]
Murakami, T [1 ]
Shiote, M [1 ]
Shiro, Y [1 ]
Hayashi, T [1 ]
Nagano, I [1 ]
Shoji, M [1 ]
Abe, K [1 ]
机构
[1] Okayama Univ, Grad Sch Med & Dent, Dept Neurol, Okayama, Japan
关键词
ALS; EAAT; glutamate; glutamate transporter; SOD1; transgenic mouse;
D O I
10.1179/016164102101200384
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The expressions of glutamate transporter proteins were immunocytochemically examined in the spinal cord of transgenic mice harboring a Gly(93) --> Ala (G93A) mutant human SOD1 gene. Astroglial EAAT2 protein level was preserved in the ventral horn even after the beginning of paralysis, and finally decreased at terminal stage of the disease (35 weeks of age), when neuronal EAAT3 protein level was also decreased. In contrast, glial fibrillary acidic protein (GFAP) immunoreactivity progressively increased from 25 weeks of age in the ventral horn. The present results show interesting dissociative expressions of astroglial proteins EAAT2 and GFAP in the same ventral horn, but suggest not an early and primary role of EAAT2 in the motoneuronal death of this model.
引用
收藏
页码:577 / 581
页数:5
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