earticle

영어

Post-traumatic stress disorder (PTSD) is a stress-related disorder that can be caused by witnessing or experiencing life-threatening events such as war, natural disaster, terrorist attack, major accidents, and assault. PTSD is caused by hippocampal malfunction and could result in problems with brain functions such as anxiety, depression, and cognitive impairments. In contrast, exercise is known to positively affect brain functions especially in the hippocampus. In this study, we investigated the effect that aerobic exercise has on the mitochondria function in the hippocampus and neuroplasticity as well as behavioral changes in animal models with PTSD. Sever stress such as PTSD resulted in impairments in mitochondrial functions in the hippocampus including the dysfunction of Ca2+ homeostasis, increase in ROS such as H2O2, and decrease in quantity of O2 respiratory. Moreover, mPTP-related proteins VDAC, ANT, and Cyp-D were overexpressed. These dysfunctions in the mitochondria of the hippocampus resulted in increased anxiety, depression, and cognitive impairment due to dysfunctions in neuroplasticity of the hippocampus such as increase in apoptosis in mitochondria and cytoplasm and decrease in BDNF and neurogenesis. Exercise improved mitochondrial functions in the hippocampus and the nerve plasticity of the hippocampus, which resulted in the alleviation of anxiety, depression, and cognitive impairments. In particular, the improvement in BDNF due to exercise can change the mitochondrial functions, neuroplasticity, and apoptosis of hippocampus which has important prevention and treatment effects on the pathobiology PTSD. Therefore, we suggest that our findings will contribute to using non-pharmaceutical physiological stimulations such as exercise preventing or protecting from stressful events.