In addition to the presynaptic A1R-mediated synaptic depression, previous studies also showed that A1R activation induced clathrin-mediated endocytosis of GluA2 subunits of AMPARs during cerebral hypoxia through the activation of p38-mitogen-activated protein kinases (p38-MAPKs) and c-Jun-N-terminal kinases (JNKs) [19,20,21]. The gene discussed is MAPK14; the disease is hypoxia.