AI Article Synopsis
- The study examined how neuroinflammation affects glutamate signaling by looking at changes in mGluR5 receptors in astrocytes exposed to substances from activated microglia.
- It found that exposure to conditioned medium from lipopolysaccharide-treated microglia led to significant changes in astrocyte characteristics and a reduction in mGluR5 expression, peaking after 48 hours.
- The influence on mGluR5 levels was linked to specific cytokines and signals from the microglia, indicating a complex interaction between these brain cells during inflammatory responses.
Article Abstract
To explore the impact of neuroinflammation on the control of glutamate transmission, we studied the metabotropic glutamate receptor 5 (mGluR5) expression in cultured astrocytes exposed to conditioned medium from lipopolysaccharide-activated microglia. This treatment caused profound changes in astrocyte phenotype that correlated with altered expression of GFAP and vimentin. This putative astrogliosis was accompanied by a down-regulation of mGluR5 protein and mRNA expression, with a maximal effect after 48 h treatment (up to 50% decrease). Such regulation was not observed with medium from naive microglia but was mimicked by direct addition of tumor necrosis factor, a major cytokine released from activated microglia. Conversely, treatment with prostaglandin E2 and induction of nitric oxide production resulted in a significant up-regulation of mGluR5. These results suggest that complex crosstalks between microglia and astrocytes during neuroinflammatory insults would influence glutamate-dependent responses in astrocytes.
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| http://dx.doi.org/10.1016/j.jneuroim.2007.06.011 | DOI Listing |
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