Tardive dyskinesia (TD) is a late-onset hyperkinetic side effect mainly affecting the orobuccal region of patients treated chronically with typical antipsychotics. In haloperidol-administered animals, we hypothesized that chronic haloperidol administration promotes faulty synaptic reorganization in a subpopulation causing a TD-like syndrome. We used the vacuous chewing movements (VCM) model of TD to investigate the expression of synaptophysin, syntaxin, spinophilm and PSD-95 in the striatum of treated animals. Male Sprague-Dawley rats were treated (12 weeks) with either haloperidol decanoate (I.M., 1mg/kg/day) or sesame oil then separated based on VCM behaviour. Using immunohistochernistry and Western Blot analysis, we found no significant effect of haloperidol (p>0.05) on protein levels. We also found no significant difference in the levels of the synaptic markers when comparing 'high' and 'low' VCM groups (p>0.05). These results suggest that synaptic alterations might not be the underlying mechanism of VCMs and possibly TD.