Unlike the inhibitory A1Rs, the lower-affinity A2AR facilitates glutamatergic neurotransmission by increasing presynaptic glutamate release as reflected by paired-pulse ratio (PPR) depression in extracellular field excitatory postsynaptic potential (fEPSP) recordings [19,21]; thus, A2AR can contribute to glutamate excitotoxicity and subsequent neuronal death in cerebral hypoxia. Here, ADORA2A is linked to hypoxia.