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L‐Glutamate Suppresses Amyloid β‐Protein‐Induced Stellation of Cultured Rat Cortical Astrocytes
Author(s) -
Abe Kazuho,
Saito Hiroshi
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.0740280.x
Subject(s) - glutamate receptor , astrocyte , stimulation , microbiology and biotechnology , neuroglia , biology , metabotropic glutamate receptor , chemistry , neuroscience , biophysics , biochemistry , receptor , central nervous system
Alzheimer’s amyloid β‐protein (Aβ) has been reported to potentiate glutamate toxicity in neurons, but very little is known about interaction between Aβ and glutamate in astrocytes. Therefore, in the present study, we investigated the effects of Aβ and glutamate on morphology of astrocytes. Cultured rat cortical astrocytes exhibited polygonal morphology in the absence of stimulation and differentiated into process‐bearing stellate cells following exposure to Aβ (20 μ M ). L‐Glutamate (30‐1,000 μ M ) had no effect on astrocyte morphology in the absence of stimulation but strongly suppressed Aβ‐induced stellation. The suppressive effect of L‐glutamate on Aβ‐induced stellation was not mimicked by glutamate receptor agonists and not blocked by glutamate receptor antagonists. In contrast, the suppressive effect of L‐glutamate was mimicked by D‐ and L‐aspartate and transportable glutamate uptake inhibitors. These results suggest that Aβ‐induced astrocyte stellation is suppressed by a mechanism related to glutamate transporters.