adaptation in dopamine D2L-mediated GluA1 trafficking in the dorsal striatum following cocaine exposure

AMPA receptor (AMPAR) plasticity at glutamatergic synapses in the mesostriatal dopaminergic pathway has beenimplicated in persistent cocaine-induced behavioral responses; however, the precise mechanism underlying thesechanges remains unknown. Utilizing cocaine psychomotor sensitization in mice we find that repeated cocaine results in abasal reduction of Ser 845 GluA1 and cell surface GluA1 levels in the dorsal striatum (dStr) following a protractedwithdrawal period, an adaptation that is dependent on Ca