Tardive dyskinesias (TD) are frequently associated with long-term antipsychotic treatment, especially in schizophrenic patients. These movement disorders have a high prevalence and can become irreversible, frequently persisting after medication is discontinued. The main hypotheses regarding the pathophysiological mechanisms underlying the development of TD include hypersensitivity of dopaminergic receptors, decreased GABAergic activity, and/or the presence of structural abnormalities in the striatum. We propose to study whether medium spiny neurons (D1- and D2-MSNs) undergo structural plastic changes after the development of TD. We established a vacuous chewing movement (VCM) model in wild type mice by administering haloperidol daily for 60 days (1.5 mg/kg for 30 days, followed by 2 mg/kg for another 30 days). Behavioral assessments were conducted throughout the treatment period and for an additional 30 days. Orofacial movements were recorded: protrusion of the tongue, wide-range chewing movements, subtle chewing movements, and jaw tremors. Mice developed low or high levels of VCM, that lasted even after the pharmacological treatment was discontinued. Using D1-tomato transgenic mice, treated with this protocol and injected with an adenoviral vector expressing GFP, we are analyzing the number of dendritic spines in MSNs. These results will allow us to determine whether the severity of VCM is associated with a differential remodeling of the dendritic spines of D1- and D2-MSNs.