Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 52, Issue 1-2, Pages 241-246Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2007.06.021
Keywords
zinc deficiency; corticosterone; calcium; spatial cognition; Schaffer collateral LTP; hippocampus
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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 corticosterome 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 Ca2+ 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. (C) 2007 Elsevier Ltd. All rights reserved.
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