On the basis of abnormal neuropsychological behavior in the open-field test after 2-week zinc deprivation, neurochemical response was examined in young mice fed a zinc-deficient diet for 2 weeks. Serum corticosterone concentration was markedly higher in zinc-deficient mice than in the control mice. Basal signals of intracellular calcium (fluo-4 FF) were also significantly more in hippocampal slices from zinc-deficient mice. These results suggest that basal Ca(2+) levels in hippocampal cells are increased by zinc deficiency. On the other hand, Schaffer collateral long-term potentiation (LTP) was unaffected by zinc deficiency; the averaged fEPSP after tetanic stimulation was 162+/-8% of baseline value in the control and 172+/-22% in zinc-deficient mice. In the Morris water maze, there was also no significant difference in learning behavior for the hidden platform task between the control and zinc-deficient mice. The present study indicates that Schaffer collateral LTP associated with spatial cognition performance are unaffected by calcium dyshomeostasis in the hippocampus elicited by 2-week zinc deprivation, which may be linked to the increased serum corticosterone concentration.
Hippocampal calcium dyshomeostasis and long-term potentiation in 2-week zinc deficiency. Publishing Authors By Initials
