Occlusal disharmony induces spatial memory impairment and hippocampal neuron degeneration via stress in SAMP8 mice

We examined the effect of occlusal disharmony in senescence-accelerated (SAMP8) mice on plasma corticosterone levels, hippocampal neuron number, and spatial performance in the water maze. The bite-raised condition was associated with an accelerated age-related decline in spatial memory, increased pl...

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Bibliographic Details
Published in:Neuroscience letters 2007-03, Vol.414 (2), p.188-191
Main Authors: Kubo, Kin-ya, Yamada, Yukiko, Iinuma, Mitsuo, Iwaku, Fumihiko, Tamura, Yasuo, Watanabe, Kazuko, Nakamura, Hiroyuki, Onozuka, Minoru
Format: Article
Language:English
Subjects:
Aging - physiology
Aging - psychology
Animals
Cell Count
Cell Death - physiology
Corticosterone - blood
Hippocampus
Hippocampus - pathology
Hippocampus - physiopathology
Male
Malocclusion - complications
Malocclusion - physiopathology
Malocclusion - psychology
Maze Learning - physiology
Memory Disorders - etiology
Memory Disorders - physiopathology
Memory Disorders - psychology
Mice
Mice, Mutant Strains
Nerve Degeneration - etiology
Nerve Degeneration - pathology
Nerve Degeneration - physiopathology
Neuronal degeneration
Occlusal disharmony
SAMP8 mice
Spatial memory
Stress
Stress, Psychological - complications
Stress, Psychological - physiopathology
Temporomandibular Joint Disorders - complications
Temporomandibular Joint Disorders - physiopathology
Temporomandibular Joint Disorders - psychology
Up-Regulation - physiology
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Summary:We examined the effect of occlusal disharmony in senescence-accelerated (SAMP8) mice on plasma corticosterone levels, hippocampal neuron number, and spatial performance in the water maze. The bite-raised condition was associated with an accelerated age-related decline in spatial memory, increased plasma corticosterone levels, and a decreased number of neurons in the hippocampal CA3 region. The findings suggest that the bite-raised condition in aged SAMP8 mice induces hippocampal neuron loss, thereby leading to senile memory deficits.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2006.12.020