Abstract
(1) Background: Depression is one of the overwhelming public health problems. Alleviating hippocampus injury may prevent depression development. Herein, we established the chronic unpredictable mild stress (CUMS) model and aimed to investigate whether aerobic exercise (AE) could alleviate CUMS induced depression-like behaviors and hippocampus injury. (2) Methods: Forty-eight healthy male Sprague-Dawley rats (200 ± 20 g) were randomly divided into 4 groups (control, CUMS, CUMS + 7 days AE, CUMS + 14 days AE). Rats with AE treatments were subjected to 45 min treadmill per day. (3) Results: AE intervention significantly improved CUMS-induced depressive behaviors, e.g., running square numbers and immobility time assessed by the open field and forced swimming test, suppressed hippocampal neuron apoptosis, reduced levels of phosphorylation of NMDA receptor and homocysteine in hippocampus, as well as serum glucocorticoids, compared to the CUMS rats. In contrast, AE upregulated phosphorylation of AMPAR receptor and brain-derived neurotrophic factor (BDNF) hippocampus in CUMS depression rats. The 14 day-AE treatment exhibited better performance than 7 day-AE on the improvement of the hippocampal function. (4) Conclusion: AE might be an efficient strategy for prevention of CUMS-induced depression via ameliorating hippocampus functions. Underlying mechanisms may be related with glutamatergic system, the neurotoxic effects of homocysteine, and/or influences in glucocorticoids-BDNF expression interaction.
Highlights
Depression emerges as one of the overwhelming public health problems [1], and patients with depression increase at an annual rate of 11.3% worldwide [2]
Strong correlations between behavioral indices and molecular alterations were observed (Figure 6B). These findings indicate that benefits of aerobic exercise (AE) on alleviating chronic unpredictable mild stress (CUMS)-induced behaviors were accomplished by its favorable regulation of hippocampal neuronal apoptosis, expression of ionotropic glutamate receptors (iGluRs), i.e., phosphorylation of AMPA receptor and phosphorylation of NMDA receptor, brain-derived neurotrophic factor (BDNF) and HCY expression in hippocampus, as well as serum level of GC
We found that AE significantly alleviated CUMS-induced depressive behaviors, suppressed hippocampal neuronal apoptosis, favorably regulated expression of iGluRs, and Exercise has been consistently recognized for its therapeutic effects on depression
Summary
Depression emerges as one of the overwhelming public health problems [1], and patients with depression increase at an annual rate of 11.3% worldwide [2]. Previous studies showed that aerobic exercise (AE) could stimulate neuron regeneration, regulate neurotrophin such as brain-derived neurotrophic factor (BDNF) and improve the plasticity of the brain [13,14]. Our recent study reported the benefits of 8 week AE on improvement of CUMS–induced depressive behavior, neuron injury, and synaptic plasticity [15]. We found that AE helped to maintain normal amplitude of population spike and fEPSP slope in CUMS rats. This finding suggests effects of AE on preventing against long-term potentiation damage caused by chronic stress
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