GRIA3 and frontotemporal dementia: By contrast, in vitro studies in rat hippocampal neuronal primary cultures and human induced pluripotent stem cell (hiPSCs)-derived neurons from FTD patients have reported that anti-AMPAR Aabs caused a reduction in GluR3-containing AMPARs via increase in endocytosis and/or increased trafficking from cell surface, together with a reduction in dendritic spine density and, ultimately, decreased glutamate release [11,18,19].