Figure 3.

(1) In Aβ_1–42-stimulated astrocytes, phosphorylation of Cx43 Ser368 residues is enhanced, resulting in a surge in hemichannel activity and ATP release. (2) A_2AR directly regulates hemichannel activity and inhibits the upregulation and phosphorylation of Cx43 in Aβ_1–42-exposed astrocytes. (3) Cx43 expression is increased in AD patients. (4) In rotenone-treated cultured astrocytes, Cx43 protein levels and phosphorylation levels were enhanced, and phosphorylated Cx43 led to gap junction cell-to-cell communication dysfunction. (5) In epilepsy, phosphorylation of Cx43 results in the release of K+ and glutamate, which increases connection conductance.