Background: Zinc is an important trace element essential for numerous bodily functions. It is believed that a deficiency of zinc can lead to various conditions, including depression, on which this study is focused. It is still not known if hypozincemia leads to the development of depression or whether zinc deficiency is a result of depression. It is hypothesized that zinc may be a therapeutic agent or supplement that would help to reverse the symptoms of this disease. Methods: In the present study, the behavior of mice was assessed 2, 4, and 10 weeks following administration of a zinc deficient diet. To evaluate animal activity we used the forced swim test (FST). Results: After 2-week zinc deprivation we demonstrated a significant reduction in the immobility time. However, after 4 and 10 weeks of zinc deprivation the mice exhibited an increased immobility time. There were no changes in locomotor activity at each time period. After 2-, 4- and 10-week zinc deprivation and the subsequent FST, serum zinc concentration was decreased and determined to be 59, 61 and 20 %, respectively, compared with appropriate controls. The serum corticosterone concentration in mice after 2-, 4- and 10-week zinc deprivation and subjected to the FST was also assessed, whereby the differences between the control and experimental animals were demonstrated (increased by: 11, 97 and 225 %, respectively). Conclusions: The obtained results indicate that zinc deprivation induced "pro-depressive" behavior (after the initial period of "antidepressive" behavior). This pro-depressive behavior correlates with enhanced serum corticosterone concentration.