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Parkinson’s disease (PD) is a progressive neurodegenerative disease,which causes a tremendous socioeconomic burden.PD patients are suffering from debilitating motor and nonmotor symptoms.Cardinal motor symptoms of PD,including akinesia,bradykinesia,resting tremor,and rigidity,are caused by the degeneration of dopaminergic neurons in the substantia nigra pars compacta.In addition,decreased amounts of dopamine (DA) level in the basal ganglia induces numerous adaptive changes at the cellular and synaptic levels in the basal ganglia circuits.These cellular and synaptic adaptations are believed to underlie the emergence and propagation of correlated,rhythmic patt of activity throughout the interconnected cortico-basal gangliathalamocortical network.The widespread pathological patt of brain activity is closely linked to the devastating motor symptoms of PD.Accumulating evidence suggests that both dopaminergic degeneration and the associated abnormal cellular and circuit activity in the basal ganglia drive the motor symptoms of PD.In this short review I summarize the recent advances in our understanding of synaptic and cellular alterations in two basal ganglia nuclei (i.e.the striatum and the subthalamic nucleus) following a complete loss of DA,and in our conceptual understanding of the cellular and circuit bases for the pathological patt of brain activity in parkinsonian state.