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L\u2010DOPA administration increased the turnover of dopamine in the striatum. L\u2010DOPA administration for 1 week produced an increase in the level of striatal RTI\u2010121 binding, a specific marker for dopamine uptake sites on the dopaminergic nerve terminals in the striatum. However, longer periods of L\u2010DOPA treatment decreased the level of RTI\u2010121 binding in the striatum. In the partial 6\u2010OHDA lesion model, L\u2010DOPA treatment had a time\u2010dependent effect on the number of neurons demonstrating a dopaminergic phenotype i.e., neurons that are tyrosine hyrdoxylase (TH)\u2010immunopositive, on the lesioned side of the brain. In the first few weeks of treatment, L\u2010DOPA decreased the number of TH\u2010positive neurons but with long\u2010term treatment, i.e., 24 weeks, L\u2010DOPA increased the number of neurons demonstrating a dopaminergic phenotype. Even in the buffered FeCl<jats:sub>3<\/jats:sub> infusion model, where the levels of iron were increased, L\u2010DOPA treatment did not have any detrimental effects on the number of TH\u2010positive neurons on the lesioned side of the brain. Consequently, chronic L\u2010DOPA treatment does not have any detrimental effects to the remaining dopaminergic neurons in rats with partial lesions to the nigrostriatal tract; indeed in the 6\u2010OHDA lesion model, long\u2010term L\u2010DOPA may increase the number of neurons, demonstrating a dopaminergic phenotype. \u00a9 2001 Movement Disorder Society.<\/jats:p>","DOI":"10.1002\/mds.1091","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T14:54:07Z","timestamp":1030287247000},"page":"424-434","source":"Crossref","is-referenced-by-count":82,"title":["Chronic L\u2010DOPA administration is not toxic to the remaining dopaminergic nigrostriatal neurons, but instead may promote their functional recovery, in rats with partial 6\u2010OHDA or FeCl<sub>3<\/sub> nigrostriatal lesions"],"prefix":"10.1002","volume":"16","author":[{"given":"Krishna 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