Endurance and resistance training mitigate the negative consequences of depression on synaptic plasticity through different molecular mechanisms

Abstract

Purpose/aim of the study: To investigate the effect and molecular mechanism of endurance and resistance training on synaptic plasticity in chronic stressed depression rats.

Materials and methods: Chronic unpredictable mild stress (CUMS) was used to establish depressive rats model. Healthy male SD rats were randomly divided into 4 groups (control, CUMS, AE, and RT). The animals in AE and RT groups were respectively subjected to continuous treadmill running and intermittent weight-bearing treadmill training for 8 weeks after CUMS. Forced swimming test (FST) was used to evaluate behavior of rats. The flow cytometry was used to detect the hippocampal neuronal apoptosis. LTP in hippocampal CA1 region were analyzed by electrophysiology. The expressions of various mRNA and proteins related to synaptic function were measured using RT-PCR, Western blot or immunohistochemistry in the hippocampus.

Results: Results shown that rats exhibited depressive behavior after CUMS stimulation, specifically immobility time was increased and swimming time and climbing time were reduced in rats during FST. After training, AE and RT all attenuated CUMS-induced depressive behavior of rats. AE and RT reduced apoptosis rate of hippocampal neuron and increased PS amplitude and fEPSPs slope after CUMS stimulation. After CUMS stimulation, AE promoted mRNA expressions, including BDNF, mTOR, TrkB, Syn, Syp, CaMKIIβ, and DRD5, and increased protein expressions, including IGF-1, PGC-1α, ERRβ, and FNDC5. While RT promoted mRNA expressions, including IGF-1, mTOR, Akt, Syn, and Syp, and improved protein expressions, including IGF-1, IGF-1R, and p-Akt.

Conclusions: In conclusion, AE and RT for 8 weeks improved CUMS-induced depressive behavior, neuron injury and synaptic plasticity through regulating different signaling pathways.

Keywords:

• Endurance exercise
• resistance exercise
• synaptic plasticity
• depression
• molecular mechanism

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by National Natural Science Foundation of China (Grant No. 81570449, 81100174).