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An increase in the subthalamic nucleus (STN) glutamatergic activity is believed to contribute to the pathophysiology of PD. However, the role of STN activity in L\u2010dopa\u2010induced motor complications is not so clear. In this study, the effect of STN lesions on L\u2010dopa\u2010induced motor response complications was investigated in rats with a nigrostriatal pathway lesion induced by 6\u2010OHDA. Animals were injected with 6\u2010OHDA in the medial forebrain bundle and treated with L\u2010dopa or saline for 22 days. On day 16, animals were randomly distributed in groups that underwent surgery in the STN ipsilateral or contralateral to 6\u2010OHDA lesion, or bilateral. Rotational behavior was measured on days 1, 15, and 22. Attenuation of STN activity by contralateral and bilateral, but not ipsilateral, STN lesion reversed the shortening in motor response duration induced by L\u2010dopa. L\u2010dopa administration, but not saline, induced prominent dyskinesias in 6\u2010OHDA\u2010lesioned rats with additional bilateral STN lesions. The results indicate that bilateral lesions of STN potentiate the duration of L\u2010dopa\u2010induced motor response and facilitate chronic L\u2010dopa\u2010induced abnormal involuntary movements in 6\u2010OHDA\u2010lesioned rats. The characteristics of the abnormal involuntary movements observed in these animals are similar to L\u2010dopa\u2010induced dyskinesias in parkinsonian patients and might be useful as an experimental model for the study of L\u2010dopa\u2010induced dyskinesia. Synapse 51:140\u2013150, 2004. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/syn.10291","type":"journal-article","created":{"date-parts":[[2003,11,12]],"date-time":"2003-11-12T14:56:39Z","timestamp":1068648999000},"page":"140-150","source":"Crossref","is-referenced-by-count":23,"title":["Bilateral subthalamic nucleus lesion reverses L\u2010dopa\u2010induced motor fluctuations and facilitates dyskinetic movements in hemiparkinsonian 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