Central administration of neuropeptide Y (NPY) produces anxiolytic-like behavioral responses in the conflict test, elevated plus maze, fear-potentiated startle paradigm, and in the chronic immobilization stress. Exogenously administrated NPY also protects against the anxiogenic effects of corticotropin-releasing factor. In the present study, we aimed to determine the effects of centrally administered NPY on the trace element disturbances in brain tissues (frontal and temporal lobes and brain stem) and the other major organs including liver, spleen (zinc [Zn]-, copper [Cu]-, and iron-rich tissues), kidney, and stomach in chronically immobilized rats. The immobilization stress was performed in special cages in which the animals were not able to move. The rats in chronic stress and chronic stress + NPY groups were kept in the cages daily for 7 min for 15 consecutive days. Intracerebroventricular (ICV) cannulas were placed to the right lateral ventricles of the rats by using stereotaxic method. In the control and chronic stress groups, 5 muL of saline (NaCl 0.9%), and in the chronic stress + NPY group, 8 mug NPY/5 muL saline solutions, were administered into the brain via ICV cannula, respectively. Controls and immobilized rats were decapitated 30 min after the injections were over and samples of tissue were taken. Zn, Cu, and iron levels of the frontal lobe, temporal lobe, brain stem, liver, spleen, kidney, and stomach were determined by flame atomic absorption spectrophotometer. Zn and Cu levels were significantly increased in the frontal lobe, temporal lobe, and brain stem in response to chronic immobilization stress daily for 7 min for 15 consecutive days. The administration of NPY inhibited the elevation of Zn in these three parts of brain but did not affect the elevation of Cu in the frontal lobe and brain stem. Increases in Zn and Cu levels of frontal, temporal lobes, and brain stem may be related to induction of MT-I mRNA expression by chronic immobilization stress, and NPY may affect this induction of MT-I, altering corticotropin-releasing factor release in the stress conditions.