Article Figures & Data
Figures
- Figure 1.
White matter neuroinflammation in a CCH rat model.
- Figure 2.
A2aR plays a bidirectional role in CCH neuroinflammation.
- Figure 3.
A2aR and mGluR5 interact to form heteromer in microglia.
- Figure 4.
High glutamate concentration promotes the formation of A2aR–mGluR5 heteromer.
- Figure 5.
High glutamate concentration promotes the formation of A2aR–mGluR5 heteromer in microglia and mediates the polarization of microglia to M1 phenotype.
- Figure 6.
A2aR–mGluR5 heteromer formation alters A2aR signaling pathway bias.
- Figure 7.
A2aR monomer activation promotes microglial polarization to M2 phenotype through Gs-mediated PKA pathway, while A2aR–mGluR5 heteromer formation mediated by glutamate concentration changes promotes microglial polarization to proinflammatory phenotype through the Gq-mediated PKC pathway.
- Figure 8.
The combination of glutamate release inhibitor (riluzole) and A2aR agonist exerts a protective effect by promoting the polarization of microglia to the M2 phenotype in the CCH model.
- Figure 9.
A graphical depiction of the dual role of A2aR in CCH.
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