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Haloperidol (HP) has been hypothesized to potentiate increases in oxidative stress or free radical\u2010mediated levels of toxic metabolites in rat striatum while simultaneous upregulating dopamine (DA)\u2010D2 receptors leading to presumed DA supersensitivity. Alpha(\u03b1)\u2010Phenyl\u2010<jats:italic>N<\/jats:italic>\u2010tert\u2010butylnitrone (PBN) is an antioxidant used to combat oxidative stress and measure increases in PBN spin\u2010adduct activity. Thus, the aim of this study was to investigate whether VCMs are related to upregulation of DA\u2010D2 receptors or to increased levels of free radicals produced during oxidative stress, and whether PBN had any protective effects. Rats received daily chronic (28 day) i.p. injections of saline, haloperidol (2 mg\/kg), PBN (150 mg\/kg), or haloperidol + PBN. The VCM model was used to measure extrapyramidal side effects of drug treatments. Electron spin resonance (ESR) spectroscopy was performed to compare concentrations of free radical species in rats receiving injections of HP + PBN. To examine the upregulation of DA\u2010D2 receptors, binding assays were carried out to assess the increase in DA\u2010D<jats:sub>2<\/jats:sub> receptor numbers with respect to VCMs following treatment of rats injected with HP, PBN, and HP + PBN. Results of these experiments show that HP\u2010induced VCMs in rats results from increases in oxidative cellular events and may not be related to increases in striatal DA\u2010D<jats:sub>2<\/jats:sub> receptors. 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