University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.
Int Rev Neurobiol. 2011;98:265-87. doi: 10.1016/B978-0-12-381328-2.00011-0.
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.
迟发性运动障碍（TD）是一种以舞蹈样、手足徐动样和节律性异常不自主运动为特征的复杂的多动综合征。尽管已经探索了各种神经保护策略来治疗 TD，但该病症仍难以治疗。各种同源、类似和相关的动物模型已经标准化，以了解 TD 的复杂神经生物学。最常见的动物模型包括向啮齿动物长期给予不同的典型神经安定药，这可能导致（i）空嚼运动，（ii）伸舌，和/或（iii）面部抽搐。预防或减少这些症状结果的药物分子被认为是抗运动障碍药物。然而，这些动物模型并不模拟确切的人类病症，并且存在一些现象学和方法学问题，因此需要临床验证。本综述将讨论这些动物模型中的一些，以探索治疗 TD 患者的新药物靶点。
