title: Glutamate receptor-mediated regulation of c-fos expression in cultured microglia.
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.
authors.affiliation: Division of Brain Diseases, Department of Biomedical Sciences, National Institute of Health, 5 Nokbun-Dong, Eunpyung-Ku, Seoul 122-701, Republic of Korea.
authors.forename: Su-Yong
authors.initials: SY
authors.lastname: Eun
authors.forename: Yun Hwa
authors.initials: YH
authors.lastname: Hong
authors.forename: Eun Hae
authors.initials: EH
authors.lastname: Kim
authors.forename: Hojeong
authors.initials: H
authors.lastname: Jeon
authors.forename: Young Ho
authors.initials: YH
authors.lastname: Suh
authors.forename: Ji Eun
authors.initials: JE
authors.lastname: Lee
authors.forename: Chulman
authors.initials: C
authors.lastname: Jo
authors.forename: Sangmee Ahn
authors.initials: SA
authors.lastname: Jo
authors.forename: Jun
authors.initials: J
authors.lastname: Kim
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D002614:Chelating Agents / Q000378:metabolism / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000378:metabolism / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000378:metabolism / Q000494:pharmacology; D005786:Gene Expression Regulation; D018698:Glutamic Acid / Q000378:metabolism / Q000494:pharmacology; D051379:Mice; D017628:Microglia / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism*; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017470:Receptors, Glutamate / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D002614:Chelating Agents; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D020033:Protein Isoforms; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D017470:Receptors, Glutamate; D014409:Tumor Necrosis Factor-alpha; D018698:Glutamic Acid; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C496318:Nos2 protein, rat; D002118:Calcium