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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.
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An examination of synaptic proteins following chronic haloperidol treatment in a rat model of tardive dyskinesia.
2006
in English
0494161892 9780494161890
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Source: Masters Abstracts International, Volume: 44-06, page: 2775.
Thesis (M.Sc.)--University of Toronto, 2006.
Electronic version licensed for access by U. of T. users.
ROBARTS MICROTEXT copy on microfiche.
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