Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8479433 | Neurochemistry International | 2008 | 6 Pages |
Abstract
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 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.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Cell Biology
Authors
Atsushi Takeda, Kohei Yamada, Haruna Tamano, Sayuri Fuke, Mika Kawamura, Naoto Oku,