Tardive dyskinesia (TD) is a complex hyperkinetic syndrome characterized by choriform, athetoid, and rhythmic abnormal involuntary movements. Even though various neuroprotective strategies have been explored for the management of TD, nevertheless, the condition is difficult to treat. Various homologous, analogous, and correlational animal models have been standardized to understand the complex neurobiology of TD. The most common animal models include chronic administration of different typical neuroleptic agents to rodents that may lead to the development of (i) vacuous chewing movements, (ii) tongue protrusions, and/or (iii) facial jerking. The drug molecules that prevent or decrease the outcome of these symptoms are considered to be antidyskinetic agents. However, these animal models do not mimic the exact human condition and possess several phenomenological and methodological problems and therefore need clinical validation. The present review will discuss some of these animal models in context of exploring the novel drug targets in treating patients suffering from TD.
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http://dx.doi.org/10.1016/B978-0-12-381328-2.00011-0 | DOI Listing |
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