This study was aimed at investigating the gene expression profile in basal ganglia of cadmium exposed rat based on cDNA array analysis. For cDNA array analysis, adult Sprague-Dawley male rats (350 ${pm}$ 25 g) were intraperitoneally injected with 2.0 mg/kg body weight/day of CdCl2 (0.3 ml) for 5 days. For doserelated gene expression analysis rats were intraperitoneally injected with 0.0, 0.1, 0.3, 1.0 mg/kg body weight/day of CdCl$_2$ for 5 days. Control rats were injected with equal volume of saline. Cadmium concentration of brain was analyzed by atomic absorption spectrophotometer. For cDNA array, RNA samples were extracted from basal ganglia and reverse-transcribed in the presence of [${alpha}$32P]-dATP. Membrane sets of the Atlas Rat 1.2 array II and Toxicology array 1.2 (Clontech, Palo Alto, CA) were hybridized with cDNA probe sets. RT-PCR was employed to validate the relative gene expression patterns obtained from the cDNA array. Northern blot hybridization methods were employed to assess the dose-related gene expression. Among the 2352 cDNAs, 671 genes were detected in both array sets and 63 genes of 38 classes showed significant (more than two fold) changes in expression. Thirty five of these genes were up-regulated and twenty eight were down-regulated in the cadmium exposed group. According to the dose-related gene expression analysis, heat shock 27 kDa protein (HSP27), neurodegeneration-associated protein 1 (Neurodap 1) genes were significantly up-regulated and melatonin receptor 1a (Mel1a), Kinesin family member 3C (KIF3C), novel kinesinrelated protein (KIF1D) genes were significantly downregulated even in the low-dose of cadmium exposed group (0.1 mg/kg body weight/day). Conclusions Sixty three genes detected in this study can give some more useful informations about the cadmium-induced neurotoxicity in the basal ganglia. As well as, HSP27, Neurodap1, Mel1a, KIF3C and KIF1D genes may be useful for the study of the cadmium-induced neurotoxicity because these genes showed dramatic changes of mRNA levels in response to the low dose of cadmium exposure.