Though a large number of animal models have revealed impaired D1R function associated with LID, including MPTP-lesioned monkeys [239,259] and 6-OHDA-lesioned rodent neurons [101,257,258]), an increasing amount of evidence indicates that D3R signaling may contribute significantly to the molecular processes underlying dyskinesia [75,76]. This evidence concerns the gene DRD1 and drug-induced dyskinesia.