A single or repeated exposure to psychostimulants induces long-lasting neuroadaptatives changes. Different neurotransmitter systems are involved in these responses including the neuropeptide angiotensin II. Our study tested the hypothesis that the neuroadaptative changes induced by amphetamine produce alterations in brain RAS components that are involve in the expression of the locomotor sensitization to the psychostimulant. Wistar male rats (250-300g), pretreated with amphetamine (5 mg/kg, ip) were used 7 or 21 days later to quantified AT₁ receptors by western blot and angiotensinogen (AOGEN) mRNA and protein in caudate putamen and accumbens nucleus. In other group of animals treated in the same way, bearing intra-cerebral cannula, the locomotor activity was tested after amphetamine challenge (0.5 mg/kg) injection and the animals received an AT₁ blocker, losartan (Los, 8 ug/ul/side) or saline 5 min before the amphetamine challenge. It was found an increase of AT₁ receptor density induced by amphetamine in both studied areas and a decrease in an AOGEN mRNA and protein only in CPu at 21 days after treatment, no changes were found in NAcc. Finally the increased locomotor activity induced by amphetamine challenge was blunted by Los administration in CPu. No statistical differences were found in the behavioral sensitization when the AT₁ blocker was injected in NAcc. Our results support the hypothesis for a key role of brain RAS in the neuroadaptative changes induced by amphetamine. More studies are needed to dissect this phenomenon.