Dopaminergic replacement as symptomatic treatment of Parkinson’s disease (PD) is effective and can be done through the administration of the dopamine precursor, L-3, 4-dihydroxyphenylalanine (L-DOPA). Continuous L- DOPA treatment is frequently associated with the development of dyskinesias. The inhibition of neuronal nitric oxide synthase (nNOS) were able to attenuate the L-DOPA-induced dyskinesias in 6-hydroydopamine (6-OHDA; Sigma-Aldrich, St. Louis, MO, USA; 24µg in 3µl saline containing 0.05% ascorbic acid) -lesioned rats. We investigated the striatal expression of inflammatory markers (cyclooxigenase-2; glial fibrilary acid protein (GFAP), and the microglia (OX-42)) on hemi-parkinsonian rats submitted to continuous treatment with L-DOPA or L-DOPA preceded by the nNOS inhibitor, 7-nitroindazol (7-NI). Methods: 6-OHDA-lesioned Wistar rats were treated daily with L-DOPA (30 mg/kg, orally by gavage) or L-DOPA plus 7-NI (30 mg/kg, ip.) over 21 days (Groups: 6-OHDA+vehicle+saline (n=6); 6-OHDA+7-NI+saline (n=3); 6-OHDA+vehicle+L-DOPA (n=7); and 6-OHDA+7-NI+L-DOPA (n=7)). Rats were examined periodically for the development of dyskinesias. The animals were anesthetized with ketamine and xylazine (100 and 10mg/kg, respectively; 1mL/kg, ip.) and submitted to transcardiac perfusion for removing the brain and carrying out the imunohistochemistry for COX-2, GFAP and OX-42. The statistical analysis was carried out by repeated two-way ANOVA followed by Tukey’s multiple comparison tests (p<0.05). Results: The continuous treatment with L-DOPA induced the expression of COX-2 in neuronal-like cells in the striatum ipsilateral to lesion (F3,22 = 130.510; P < 0.001). We also observe that the COX-2-immunoreactivity in the striatum co-localize with cAMP-regulated phosphoprotein (DARPP-32), choline acetyltransferase (ChAT) and calbindin neurons bud not with calretinin, parvalbumin and nNOS immunolabeling. Furthermore, L-DOPA also induced an increase in the density of nitric oxide synthase in neuronal cells (F3,22 = 7.199; P < 0.001), astrocytes (F3,22 = 20.211; P < 0.001), and microglial cells (F3,22 = 20.620; P < 0.001) compared to vehicle+saline group. In the same way as dyskinesias, all these cellular alterations were prevented by the pre-treatment of animals with the nNOS inhibitor 7-NI (COX-2 (F3,22 = 130.510; P < 0.001); nNOS (F3,22 = 7.199; P = 0.001); GFAP (F3,22 = 20.211; P < 0.001) and OX-42, F3,22 = 20.620; P < 0.001)). Conclusion: The major finding of this study was the parallel of L-DOPA-induced dyskinesias with expression of COX-2 in the striatum, as well astrocytic and microglial cells. Moreover, 7-NI prevented the striatal cellular changes, without harming its beneficial effects in dyskinetic rats. This outcome appears to involve striatal interneurons, projection neurons and the direct pathway.