Parkinson’s disease (PD) is a chronic neurodegenerative disorder characterized by the preferential loss of dopaminergic neurons stemming from the substantia nigra pars compacta and innervating the dorsal striatum. The substantial decreases in striatal dopamine (DA) result in devastating hypokinetic movements and motor disturbances. Increased generation of reactive oxygen species, such as hydrogen peroxide (H₂O₂), is also thought to contribute to Parkinsonian symptoms. However, the precise role of H₂O₂ in the initiation, progression, and maintenance of the disease remains unclear, as reactive oxygen species are difficult to monitor in brain tissue. Further, several lines of evidence suggest that the standard treatment strategy of dopaminergic replacement therapy via administration of Levodopa (L-DOPA; L-3,4 dihydroxyphenylalanine) may serve to increase oxidative stress and potentiate cell death. We are investigating how striatal H₂O₂ and DA dynamics underlie behavioral changes that result from chronic L-DOPA administration in a rodent model of PD (unilateral 6-OHDA lesion) using fast-scan cyclic voltammetry, an electrochemical technique that affords precise spatial and temporal resolution, as well as selective detection of these neurochemicals. Specifically, carbon-fiber microelectrodes are used to simultaneously quantify rapid H₂O₂ and DA fluctuations at single recording sites in the dorsal striatum over several weeks of L-DOPA administration. The chemical fluctuations are correlated with behavioral abnormalities that develop over the course of treatment. These studies are advancing our understanding of how oxidative stress modulates nigrostriatal DA signaling, and are demonstrating how these signals correspond with dyskinetic movements in the treatment of PD.