IADR Abstract Archives
Effect of molerless induced learning impairment by the enriched environment in mouse
Objectives: Impaired mastication is an epidemiologic risk factor for learning deficits. Intervention programs for demented persons that include exercise and participation in hobbies slow the progression of dementia. Tooth extraction (molarless condition) accelerates spatial learning deficits and suppresses neurogenesis in the hippocampal dentate gyrus (DG) in mice. Exposure to an enriched environment (EE) enhances hippocampal neurogenesis and brain-derived neurotrophic factor (BDNF) expression, and improves cognitive function. We examined the effects of EE exposure on BDNF protein expression levels using an enzyme-linked immunosorbent assay, neurogenesis in the hippocampal DG, and learning ability in molarless mice.
Methods: The mice were divided into four groups: Control/standard environment (SE), molarless/SE, control/EE, and molarless/EE. For EE exposure, mice were housed in a large cage and provided access to objects such as toys, a running wheel, and plastic tunnels. The SE mice were housed in standard cages without these objects. The mice were housed in the SE or EE conditions for 3 weeks.
Results: In molarless/SE mice, neurogenesis in the hippocampal DG and BDNF protein expression in the hippocampus were reduced, and learning was impaired compared to control/SE mice. In molarless/EE mice, however, the suppression of neurogenesis and decreased BDNF protein expression were attenuated, and the learning impairment was reduced compared to molarless/SE mice.
Conclusion: These findings suggest that EE ameliorates the molarless-induced suppression of BDNF in the hippocampus, which in turn reduces the decrease in hippocampal neurogenesis and learning ability.
Conclusions: In molarless/SE mice, neurogenesis in the hippocampal DG and BDNF protein expression in the hippocampus were reduced, and learning was impaired compared to control/SE mice. In molarless/EE mice, however, the suppression of neurogenesis and decreased BDNF protein expression were attenuated, and the learning impairment was reduced compared to molarless/SE mice.
Conclusion: These findings suggest that EE ameliorates the molarless-induced suppression of BDNF in the hippocampus, which in turn reduces the decrease in hippocampal neurogenesis and learning ability.
Methods: The mice were divided into four groups: Control/standard environment (SE), molarless/SE, control/EE, and molarless/EE. For EE exposure, mice were housed in a large cage and provided access to objects such as toys, a running wheel, and plastic tunnels. The SE mice were housed in standard cages without these objects. The mice were housed in the SE or EE conditions for 3 weeks.
Results: In molarless/SE mice, neurogenesis in the hippocampal DG and BDNF protein expression in the hippocampus were reduced, and learning was impaired compared to control/SE mice. In molarless/EE mice, however, the suppression of neurogenesis and decreased BDNF protein expression were attenuated, and the learning impairment was reduced compared to molarless/SE mice.
Conclusion: These findings suggest that EE ameliorates the molarless-induced suppression of BDNF in the hippocampus, which in turn reduces the decrease in hippocampal neurogenesis and learning ability.
Conclusions: In molarless/SE mice, neurogenesis in the hippocampal DG and BDNF protein expression in the hippocampus were reduced, and learning was impaired compared to control/SE mice. In molarless/EE mice, however, the suppression of neurogenesis and decreased BDNF protein expression were attenuated, and the learning impairment was reduced compared to molarless/SE mice.
Conclusion: These findings suggest that EE ameliorates the molarless-induced suppression of BDNF in the hippocampus, which in turn reduces the decrease in hippocampal neurogenesis and learning ability.