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KMID : 1101720150190030191
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Physical Activity and Nutrition
2015 Volume.19 No. 3 p.191 ~ p.197
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Exercise copes with prolonged stress-induced impairment of spatial memory performance by endoplasmic reticulum stress
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Kang Jong-Seok
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Abstract
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The present study demonstrates that prolonged restraint administration for 21 days caused memory impairment and induced hippocampal endoplasmic reticulum (ER) stress-mediated apoptosis. On the contrary, this change was revered by treadmill running for 8 weeks. Repeated psychological stress caused an increase in escape latency time in the water maze test, accompanied by the induction of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), and cleaved/active caspase-12 protein in the hippocampus. The expression pattern of ER stress response-related proteins were counter-regulated by chronic exercise, as indicated by a reduction in GRP78, CHOP, and cleaved caspase-12, along with a decrease in escape latency time. In addition, the hippocampal expression pattern of phospho-cAMP response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) opposed that of ER stress response components. Accordingly, chronic exercise may attenuate prolonged stress-induced hippocampal ER stress and memory deficit, likely through CREB/BDNF signaling.
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KEYWORD
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prolonged stress, exercise, endoplasmic reticulum stress, glucose-regulated protein 78, CHOP, memory
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