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Glutamate activates c‐fos in glial cells via a novel mechanism involving the glutamate receptor subtype mGlu5 and the transcriptional repressor DREAM by Ylva Edling; Magnus Ingelman‐Sundberg; Anastasia Simi is a Neuroscience article available to read on EtoBox.

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## Abstract Activation of __c‐fos__ in brain is related to coupling of neuronal activity to gene expression, but also to pathological conditions such as seizures or excitotoxicity‐induced cell death. Glutamate activates __c‐fos__ in neurons through the calcium‐dependent phosphorylation of CREB by ERK and/or CaMKIV kinase pathways downstream NMDA‐receptors. In glial cells, however, the activation of __c‐fos__ by glutamate is poorly understood. Because glial cells actively modulate neuronal excitability and the brain's response to injury, we studied the mechanisms by which glutamate activates __c‐fos__ in rat cortical glial cells. Glutamate potently induced c‐fos mRNA in a calcium‐dependent manner, as demonstrated by using the calcium chelator BAPTA‐AM. Glutamate‐induced c‐fos mRNA expression was not sensitive to inhibitors of ERK, p38^MAPK^, or CaMK pathways, indicating that glial __c‐fos__ is activated by a distinct mechanism. Thapsigargin abolished the glutamate effect on c‐fos mRNA, indicating ER calcium mobilization. Additionally, glutamate induction of c‐fos mRNA was sensitive to the mGluR5 antagonist MPEP but not the NMDA‐R antagonist MK‐801. In luciferase reporter assays, __D

Who reads Glutamate activates c‐fos in glial cells via a novel mechanism involving the glutamate receptor subtype mGlu5 and the transcriptional repressor DREAM?

Author

Ylva Edling; Magnus Ingelman‐Sundberg; Anastasia Simi

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square (ISSN 0894-1491)

Published

2006

Language

EN

Field

Neuroscience (Life Sciences)