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We examined the role of AMPAR insertion\/anchoring in basal synaptic transmission. Perfusion of an inhibitor of synaptotagmin-soluble n-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor SNARE-mediated exocytosis depressed basal EPSC amplitudes, whereas a peptide that inhibits GluR2\/3 interactions with postsynaptic density-95 (PDZ) domain proteins glutamate receptor interacting protein (GRIP)\/protein interacting with C-kinase-1 (PICK1) enhanced basal synaptic transmission. These results suggest that constitutive trafficking and anchoring of AMPARs help maintain basal synaptic transmission. The regulation of postsynaptic AMPAR trafficking involves synaptotagmin-SNARE-mediated vesicle exocytosis and interactions between AMPARs and the PDZ domains in GRIP\/PICK1. We show that inhibitors of synaptotagmin-SNARE-mediated exocytosis, or interactions between AMPARs and GRIP\/PICK1, attenuated AdA-enhanced increases in EPSC amplitudes. These results suggest that IP<jats:sub>3<\/jats:sub>R-mediated Ca<jats:sup>2+<\/jats:sup>release can enhance AMPAR EPSC amplitudes through mechanisms that involve AMPAR-PDZ interactions and\/or synaptotagmin-SNARE-mediated receptor trafficking.<\/jats:p>","DOI":"10.1152\/jn.00651.2004","type":"journal-article","created":{"date-parts":[[2004,12,16]],"date-time":"2004-12-16T23:18:14Z","timestamp":1103239094000},"page":"178-188","source":"Crossref","is-referenced-by-count":12,"title":["Activation of Postsynaptic Ca<sup>2+<\/sup>Stores Modulates Glutamate Receptor Cycling in Hippocampal Neurons"],"prefix":"10.1152","volume":"93","author":[{"given":"Brady J.","family":"Maher","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"II","given":"Roger 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