GPR88 and drug-induced dyskinesia: Thus, the lack of dyskinesia development and the lack of aggravation of AIMs after the dorso-striatal inactivation of Gpr88 suggest that, while the KD-Gpr88 may act by hyperactivating the D1 direct pathway through the induction of ΔFosB, this effect is not directly coupled to dyskinetic effects even during a chronic L-DOPA treatment.