An Animal Model to Study the Molecular Basis of Tardive Dyskinesia
Long-term treatment with haloperidol is associated with a number of extrapyramidal side effects. This limitation presents a marked therapeutic challenge. The present method (21 days administration of haloperidol, 5 mg/kg, i.p.) has been established to gain deeper insight into the molecular etiology (inflammation and apoptosis) of haloperidol-induced cellular death. In the present model, besides the corresponding increase in the vacuous chewing movements (VCMs), enhanced oxidative stress, there was a significant increase in cellular markers of inflammation and apoptotic protein (caspase-3), leading to cellular death. We also suggest that this model will be effective in preclinical testing of new chemical entities for the treatment of haloperidol induced tardive dyskinesia and related symptoms.
Key wordsApoptosis Caspase-3 Haloperidol Inflammation Oxidative damage Tardive dyskinesia
The authors would like to thank Professor S.K. Kulkarni and Dr. Kanwaljit Chopra for their guidance and support.
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