Enriched environment ameliorates molarless-induced learning impairment
Hiroko Kondo1), Minori Kurahashi1), Ayumi suzuki1),Mika Onishi1),
Chika Murabayashi1), Mitsuo Iinuma1), Daisuke Mori2), Huayue Chen3),
Kin-ya Kubo4)
1) Dept. Pediatric Dent., Asahi Univ. Sch. Dent.
2) Dept. Prosthodontics., Asahi Univ. Sch. Dent.
3) Gifu Univ. Sch. Med.
4) Seijoh Univ. Grad. Sch. Health Care Studies
Impaired mastication is an epidemiologic risk factor for learning deficits. Intervention programs for demented older persons that include exercise and participation in hobbies slow the progression of dementia. Tooth extraction (molarless condition) accelerates age-related spatial learning deficits and suppresses cell proliferation in the hippocampal dentate gyrus (DG) in senescence-accelerated prone mice (SAMP8). Exposure to an enriched environment (EE) enhances hippocampal cell proliferation and brain-derived neurotrophic factor (BDNF) expression, and improves cognitive function. Here we examined the effects of exposure to an EE on BDNF protein expression levels by an enzyme-linked immunosorbent assay, cell proliferation in the hippocampal DG, and learning ability in molarless aged SAMP8 mice.
The mice were divided into four groups: Control/standard environment (SE), molarless/SE, control/EE, 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 toys, running wheels, or plastic tunnels. The mice were housed in the SE or EE conditions for a period of 3 weeks.
In molarless/SE mice, cell proliferation in the hippocampal DG and BDNF protein expression in the hippocampus were reduced, and learning was impaired compared to control/SE mice. Molarless/EE mice, however, had attenuated suppression of cell proliferation and BDNF protein expression, and the learning impairment was reduced compared to molarless/SE mice. 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.