Swimming exercise reduces the vulnerability to stress and contributes to the AKT/GSK313/CRMP2 pathway and microtubule dynamics mediated protective effects on neuroplasticity in male C57BL/6 mice

While swimming exercise has been shown to positively affect the development of the nervous system, it still remains unclear whether it reduces the vulnerability to stress. In this study, male C57BL/6 mice were exposed to swimming training for 5 weeks, and then subjected to chronic unpredictable mild stress (CUMS) for 4 weeks. We found that swimming exercise prevented anxiety-like and depressive phenotypes induced by CUMS, including increased anxiety-like behavior in the open field test (OFT) and elevated plus-maze (EPM) test and increased despair behavior in the tail suspension test (TST). Moreover, the control+stress group showed reduced expression of phosphorylated AKT kinase (p-AKT), phosphorylated glycogen synthase kinase-313 (p-GSK313), and tubulin-tyrosine ligase (Tyr-tubulin) and increased protein expression of phosphorylated collapsin response mediator protein 2 (p-CRMP-2); the control+control, swim+control, and swim+stress groups exhibited higher expression of these proteins than the control+stress group. This study confirmed that swimming exercise could reduce the vulnerability of individuals to stress and that it contributes to the AKT/GSK-313/CRMP-2 pathway and microtubule dynamics mediated protective effects on neuroplasticity. The AKT/GSK-313/CRMP-2 pathway and microtubule dynamics may be involved in resilience to stress.