Abstract
The expressions of glutamate transporter proteins were immunocytochemically examined in the spinal cord of transgenic mice harboring a Gly93 --> 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.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Transport System X-AG / metabolism*
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Amyotrophic Lateral Sclerosis / genetics
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Amyotrophic Lateral Sclerosis / metabolism
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Amyotrophic Lateral Sclerosis / pathology
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Animals
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Astrocytes / metabolism*
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Excitatory Amino Acid Transporter 2 / metabolism
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Glial Fibrillary Acidic Protein / metabolism
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Immunohistochemistry
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Matched-Pair Analysis
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Mice
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Mice, Transgenic
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Spinal Cord / cytology
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Spinal Cord / metabolism*
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Superoxide Dismutase / genetics
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Superoxide Dismutase-1
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Time Factors
Substances
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Amino Acid Transport System X-AG
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Excitatory Amino Acid Transporter 2
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Glial Fibrillary Acidic Protein
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SOD1 protein, human
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Sod1 protein, mouse
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Superoxide Dismutase
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Superoxide Dismutase-1