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The first animal models of peak\u2010dose <jats:sc>l<\/jats:sc>\u2010dopa\u2010induced dyskinesia were produced in monkeys lesioned with N\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP) and treated chronically with <jats:sc>l<\/jats:sc>\u2010dopa to elicit choreic movements and dystonic postures. Seminal studies were performed in these models using both metabolic mapping and electrophysiological techniques, providing fundamental pathophysiological insights that have stood the test of time. A decade later, it was shown possible to reproduce peak\u2010dose <jats:sc>l<\/jats:sc>\u2010dopa\u2010induced dyskinesia in rats and mice rendered parkinsonian with nigrostriatal 6\u2010hydroxydopamine lesions. When treated with <jats:sc>l<\/jats:sc>\u2010dopa, these animals exhibit abnormal involuntary movements having both hyperkinetic and dystonic components. These models have enabled molecular\u2010 and cellular\u2010level investigations into the mechanisms of <jats:sc>l<\/jats:sc>\u2010dopa\u2010induced dyskinesia. A flourishing literature using genetically engineered mice is now unraveling the role of specific genes and neural circuits in the development of <jats:sc>l<\/jats:sc>\u2010dopa\u2010induced motor complications. Both non\u2010human primate and rodent models of peak\u2010dose <jats:sc>l<\/jats:sc>\u2010dopa\u2010induced dyskinesia have excellent construct validity and provide valuable tools for discovering therapeutic targets and evaluating potential treatments. \u00a9 2018 International Parkinson and Movement Disorder Society<\/jats:p>","DOI":"10.1002\/mds.27337","type":"journal-article","created":{"date-parts":[[2018,2,28]],"date-time":"2018-02-28T04:35:12Z","timestamp":1519792512000},"page":"889-899","source":"Crossref","is-referenced-by-count":106,"title":["Animal models of <scp>l<\/scp>\u2010dopa\u2010induced dyskinesia in Parkinson's disease"],"prefix":"10.1002","volume":"33","author":[{"given":"M. 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