The Rodent Models of Dyskinesia and Their Behavioral Assessment

Dyskinesia, a major motor complication resulting from dopamine replacement treatment, manifests as involuntary hyperkinetic or dystonic movements. This condition poses a challenge to the treatment of Parkinson's disease. So far, several behavioral models based on rodent with dyskinesia have bee...

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Published inFrontiers in neurology Vol. 10; p. 1016
Main Authors Peng, Qiwei, Zhong, Shaoping, Tan, Yang, Zeng, WeiQi, Wang, Ji, Cheng, Chi, Yang, Xiaoman, Wu, Yi, Cao, Xuebing, Xu, Yan
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 11.10.2019
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Summary:Dyskinesia, a major motor complication resulting from dopamine replacement treatment, manifests as involuntary hyperkinetic or dystonic movements. This condition poses a challenge to the treatment of Parkinson's disease. So far, several behavioral models based on rodent with dyskinesia have been established. These models have provided an important platform for evaluating the curative effect of drugs at the preclinical research level over the past two decades. However, there are differences in the modeling and behavioral testing procedures among various laboratories that adversely affect the rat and mouse models as credible experimental tools in this field. This article systematically reviews the history, the pros and cons, and the controversies surrounding rodent models of dyskinesia as well as their behavioral assessment protocols. A summary of factors that influence the behavioral assessment in the rodent dyskinesia models is also presented, including the degree of dopamine denervation, stereotaxic lesion sites, drug regimen, monitoring styles, priming effect, and individual and strain differences. Besides, recent breakthroughs like the genetic mouse models and the bilateral intoxication models for dyskinesia are also discussed.
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This article was submitted to Movement Disorders, a section of the journal Frontiers in Neurology
Reviewed by: Barbara Picconi, Università Telematica San Raffaele, Italy; M. Angela Cenci, Lund University, Sweden
Edited by: Alain Kaelin-Lang, Neurocenter of Southern Switzerland (NSI), Switzerland
These authors have contributed equally to this work as co-first authors
Present address: Shaoping Zhong, Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China
ISSN:1664-2295
1664-2295
DOI:10.3389/fneur.2019.01016