Significance of serum glucocorticoid and chelatable zinc in depression and cognition in zinc deficiency.

Abstract Dietary zinc deficiency elicits neuropsychological symptoms and cognitive dysfunction. To pursue the mechanisms of these symptoms, in the present study, the relationship among serum glucocorticoid, chelatable zinc in the synaptic cleft and brain function based on behavior was examined in young rats fed a zinc-deficient diet for 4 weeks. Serum glucocorticoid level was significantly increased in zinc-deficient rats. However, the induction of in vivo dentate gyrus LTP and object recognition memory were not affected in zinc-deficient rats. Chelatable zinc levels were decreased in the stratum lucidum of the hippocampal CA3, but not in the molecular layer of the dentate gyrus. It is reported that dentate gyrus LTP and object recognition memory are affected in clioquinol (30 mg/kg)-administered rats, in which chelatable zinc is significantly decreased in the molecular layer of the dentate gyrus. Thus, the significant decrease in chelatable zinc in the molecular layer of the dentate gyrus may be required for object recognition memory deficit in zinc deficiency. On the other hand, the time of grooming in the open-field test was decreased in zinc-deficient rats. Immobility time in the forced swim test was increased in zinc-deficient rats, but not in clioquinol-administered rats, in which chelatable zinc was more markedly decreased than in zinc-deficient rats, suggesting that the lack of chelatable zinc does not increase depression-like behavior. These results suggest that the chronic increase in serum glucocorticoid level is involved in the increase in depression-like behavior rather than the decrease in chelatable zinc after 4-week zinc deficiency.