Exercise copes with prolonged stress-induced impairment of spatial memory performance by endoplasmic reticulum stress

Exercise copes with prolonged stress-induced impairment of spatial memory performance by endoplasmic reticulum stress

Jong-Seok Kang. Exercise copes with prolonged stress-induced impairment of spatial memory performance by endoplasmic reticulum stress. JENB., Vol. 19, No. 3, pp.191-197, 2015 [Purpose] 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. [Key words] prolonged stress, exercise, endoplasmic reticulum stress, glucose-regulated protein 78, CHOP, memory

Jong-Seok Kang. Exercise copes with prolonged stress-induced impairment of spatial memory performance by endoplasmic reticulum stress. JENB., Vol. 19, No. 3, pp.191-197, 2015 [Purpose] 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. [Key words] prolonged stress, exercise, endoplasmic reticulum stress, glucose-regulated protein 78, CHOP, memory