2012 Volume 22 Issue 2 Pages 110-116
Early toothlessness in senescence-accelerated prone (SAMP8) mice leads to increased plasma corticosterone levels, learning deficits, neuronal death, and increased astroglial responsiveness in the hippocampus. New cells are generated in the hippocampal dentate gyrus (DG) throughout life in animals as well as humans. Neurogenesis in the hippocampal DG is sensitive to glucocorticoid levels and environmental triggers such as learning. Here we investigated the mechanisms underlying impaired hippocampal function resulting from early masticatory dysfunction, by examining the effects of tooth loss soon after tooth eruption on plasma corticosterone levels, learning ability in the Morris water maze test, and cell proliferation in the hippocampal DG of 1-, 5-, and 9-mo-old SAMP8 mice. Bromodeoxyuridine, a marker of newborn cells, was injected, and BrdU-positive cells were quantitatively analyzed to detect cell proliferation in the hippocampal DG using immunohistochemical techniques. Early toothlessness enhanced the age-related increase in plasma corticosterone levels and learning deficits, and led to a decrease in the number of BrdU-positive cells in the hippocampal DG. Plasma corticosterone levels, learning deficits, and the number of BrdU-positive cells in the hippocampal DG was significantly different between in 5- and 9-mo-old early toothless mice and age-matched control mice, but not between 1-mo-old early toothless mice and controls. These findings suggest that early toothlessness leads to increased plasma corticosterone levels and a decrease in cell proliferation in the hippocampal DG, thereby leading to learning deficits.
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