Abstract
It has been recently shown that the expression of various types of neurotransmitter receptors is not restricted to neurons but also observed in a majority of glial cells. However, their function in glial cells is not known well in both physiological and pathological conditions. Here, we investigated the role of glutamate receptor on c-fos gene expression in primary cultured and BV-2 microglia. Our results demonstrated that both c-fos mRNA and protein were dramatically induced following treatment with various glutamate receptor agonists (500muM); N-methyl-d-aspartic acid, kainic acid, (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and (RS)-3,5-dihydroxyphenylglycine. The responses were significantly suppressed by specific antagonists and also by calcium chelating agents EGTA and BAPTA-AM. Our results suggest that glutamate receptor activation regulates c-fos gene expression by modifying intracellular calcium levels in microglia. These findings might provide an insight in to understanding the function of microglial glutamate receptors in neuron-to-glial interaction under the excitotoxic conditions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Calcium / metabolism
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Cells, Cultured
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Chelating Agents / metabolism
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Chelating Agents / pharmacology
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Excitatory Amino Acid Agonists / metabolism
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Excitatory Amino Acid Agonists / pharmacology
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Excitatory Amino Acid Antagonists / metabolism
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Excitatory Amino Acid Antagonists / pharmacology
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Gene Expression Regulation*
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Glutamic Acid / metabolism
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Glutamic Acid / pharmacology
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Mice
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Microglia / cytology
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Microglia / drug effects
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Microglia / physiology*
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Nitric Oxide Synthase / genetics
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Nitric Oxide Synthase / metabolism
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Nitric Oxide Synthase Type II
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Protein Isoforms / genetics
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Protein Isoforms / metabolism
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Proto-Oncogene Proteins c-fos / genetics
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Proto-Oncogene Proteins c-fos / metabolism*
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Proto-Oncogene Proteins c-jun / genetics
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Proto-Oncogene Proteins c-jun / metabolism
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Rats
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Rats, Sprague-Dawley
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Receptors, Glutamate / metabolism*
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Chelating Agents
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Excitatory Amino Acid Agonists
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Excitatory Amino Acid Antagonists
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Protein Isoforms
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Proto-Oncogene Proteins c-fos
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Proto-Oncogene Proteins c-jun
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Receptors, Glutamate
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Tumor Necrosis Factor-alpha
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Glutamic Acid
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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Nos2 protein, rat
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Calcium