Fig 2: Schematic representation of the changes observed in the glutamatergic synapse in the PFC of DAT−/− rats. The condition of hyperdopaminergia caused by DAT deletion alters the trafficking of AMPA receptors and their scaffolding protein expression. Changes in the endosomal and autophagic mechanisms are paralleled with the impairment of the glutamatergic synapse. AMPA, glutamate-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors; SAP97, synapse-associated protein 97; GRIP, glutamate receptor-interacting protein; PSD95. postsynaptic density protein 95; Arc/Arg3.1, Activity-regulated cytoskeleton-associated protein; Rab5, Ras-associated binding protein 5; Rab9, Ras-associated binding protein 9; LC3-II, microtubule-associated proteins 1A/1B light chain 3B; EE, early endosome; LE, late endosome; A, autophagosome.