| 노화 쥐 해마 CA1에서의 운동을 통한 BDNF 발현 유도 및 PI3K/AKT에 의한 synaptic 단백질 발현 |
| 어수주1, 김동문2 |
1한국체육대학교
2원광대학교 |
| The Exercise-induced BDNF and synaptic proteins via PI3K/AKT on Hippocampal CA1 in aged mice. |
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| ABSTRACT |
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We identified whether the 8 week-period of treadmill running might induce BDNF and pre- and post-synaptic proteins on hippocamapl CA1 in aged mice, and whether PI3K/AKT pathway might be involved to the exercise-induced BDNF signaling. To achieve our objective, mice were divided into two groups (CON, EX). Mice were subjected to treadmill-running for 8 weeks of period (19 m/min, 60 min/day, 5 days/week). First, the immunoreactivities of BDNF protein were lower in aged mice (60 wk of age) than that in young mice (10 wk of age) on hippocampal CA1 region (p<.05) measured by immunohistochemistry. Next, the reduced levels of BDNF expression in aged mice were significantly reserved in response to exercise (p<.05), and tPA expression levels were enhanced exposed by exercise administration measured by immunohistochemistry and western blot analysis (p<.05). The expression levels of pre- and post-synaptic proteins such as SNAP25, snaptophysin, PSD95, NR2B were profoundly increased in exercised aged mice compared with sedentary mice (p<.05, respectively) assessed by western blot analysis. Finally, The immunoreactivities of p-PI3K and p-AKT protein were remarkedly enhanced in response to exercise assessed by western blot (p<.05, respectively). Collectively, the administrated exercise paradigm in the current study induced BDNF expression, and BDNF/PI3K/AKT signaling cascade was activated, thereby enhancing pre- and post-synatic proteins expression and neurosynaptic plasticity on hippocampal CA1 region in aged mice. Accordingly, the regular and long-term endurence exercise can exert a beneficial effect on age-related decline of learning, memory, and cognitive function as well as neurodegenerative disease including Alzheimer's disease. |
| Key words:
BDNF, Neurosynaptic, Treadmill running, PI3K/AKT, Hippocampal CA1 |
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