ADORA2A and brain ischemia: Recently, we showed that prolonged A1R stimulation during the hypoxic/reperfusion injury model caused upregulation of calcium-permeable AMPARs, synaptic potentiation, and hippocampal neuronal damage resulting from signaling interactions between A1R and A2AR [31]; thus, blocking AMPARs can be a potential target to prevent cerebral ischemia-induced neurodegeneration.