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However, the impact of this treatment on glutamate transmission in the basal ganglia has been poorly investigated. In this study, we examined the effects of 6\u2010hydroxydopamine\u2010induced lesion of nigral dopamine neurons with or without subsequent chronic <jats:sc>l<\/jats:sc>\u2010DOPA treatment on several parameters of glutamate system function in the rat striatum and substantia nigra pars reticulata. All the lesioned animals treated with <jats:sc>l<\/jats:sc>\u2010DOPA developed severe dyskinesias. Extracellular glutamate levels, measured by microdialysis in freely moving conditions, and gene expression of the glial glutamate transporter GLT1, assessed by <jats:italic>in situ<\/jats:italic> hybridization, were unaffected by dopamine lesion or <jats:sc>l<\/jats:sc>\u2010DOPA treatment alone, but were both markedly increased on the lesion side of rats with subsequent <jats:sc>l<\/jats:sc>\u2010DOPA treatment. No change in the expression of the vesicular glutamate transporters vGluT1 and vGluT2 was measured in striatum. These data show that chronic <jats:sc>l<\/jats:sc>\u2010DOPA treatment leading to dyskinesias increases basal levels of glutamate function in basal ganglia. The <jats:sc>l<\/jats:sc>\u2010DOPA\u2010induced overexpression of GLT1 may represent a compensatory mechanism involving astrocytes to limit glutamate overactivity and subsequent toxic processes.<\/jats:p>","DOI":"10.1111\/j.1460-9568.2004.03591.x","type":"journal-article","created":{"date-parts":[[2004,9,1]],"date-time":"2004-09-01T15:29:43Z","timestamp":1094052583000},"page":"1255-1266","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":122,"title":["Chronic <scp>l<\/scp>\u2010DOPA treatment increases extracellular glutamate levels and GLT1 expression in the basal ganglia in a rat model of Parkinson's disease"],"prefix":"10.1111","volume":"20","author":[{"given":"S.","family":"Robelet","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Melon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.","family":"Guillet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Salin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Kerkerian\u2010Le Goff","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2004,9]]},"reference":[{"key":"e_1_2_25_2_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00970540"},{"key":"e_1_2_25_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/PL00007767"},{"key":"e_1_2_25_4_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-20-09134.2002"},{"key":"e_1_2_25_5_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-21-08648.1998"},{"key":"e_1_2_25_6_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9568.2003.02795.x"},{"key":"e_1_2_25_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(97)00033-4"},{"key":"e_1_2_25_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0149-7634(96)00032-2"},{"key":"e_1_2_25_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"e_1_2_25_10_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/116.2.433"},{"key":"e_1_2_25_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1353-8020(02)00029-9"},{"key":"e_1_2_25_12_1","first-page":"70","article-title":"Molecular basis of levodopa\u2010induced dyskinesias","volume":"47","author":"Calon F.","year":"2000","journal-title":"Ann. 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