Mechanisms of dyskinesias including L-DOPA-induced peak dose dyskinesia (LID) and neuroleptics-induced tardive dyskinesia (TD) have not been clearly elucidated. According to pioneering animal works done by Dr. Tomiyama at Hirosaki University, it is now known that terminals of striatal medium spiny neurons enlarged and as a result the volume of globus pallidus and sustantia nigra increased in LID rodent models. We examined if these anatomical changes were also seen in TD and sought to address shared molecular mechanisms in dyskinesias. Through pharmacological and neurochemical interventions, we found increase GABA transmission in basal ganglia in dyskinesia-animal models. This abnormality may be a potential therapeutic target.