High-Intensity Interval Training on Neuroplasticity, Balance between Brain-Derived Neurotrophic Factor and Precursor Brain-Derived Neurotrophic Factor in Poststroke Depression Rats.

BACKGROUND: High-intensity interval training (HIIT) improves functional and mental health in the patients with stroke. To investigate the potential mechanisms of HIIT on poststroke depression (PSD).

METHODS: Wistar rats were randomly divided into control, Sham, PSD, moderate intensity continuous training (MICT), and HIIT groups. After PSD model was successful made, the maximum speed (Smax) and the blood lactate threshold corresponding speed (SLT ) were measured. Different intensity training protocols were performed on the MICT and HIIT groups, respectively. The behavioral tests (open field, forced swimming, and sucrose preference tests) were performed before and after training. Nissl staining was used to observe the changes of neuronal cell morphology in the left hippocampus. The expression of mature brain-derived neurotrophic factor (mBDNF), tropomyosin receptor kinase B (TrkB), precursor BDNF (proBDNF), pan-neurotrophin receptor 75 (p75NTR), NR2A, NR2B proteins, and BDNF, tissue plasminogen activator (tPA) mRNA in the hippocampus were detected by Western blotting, immunohistochemistry or RT-PCR after training.

RESULTS: After 28 days of training, higher center occupancy, immobility time, and level of proBDNF, p75NTR, and NR2B proteins, lower sucrose preference and level of mBDNF, TrkB, NR2A proteins, and BDNF, tPA mRNA were observed in the PSD group. Neuronal cells and Nissl body in the hippocampus were loosely arranged and lightly stained in the PSD group. The ethological findings, Nissl staining especially in the CA1 and dentate gyrus areas, expression of proteins and mRNA above in the MICT and HIIT rats were reversed. And the HIIT group changed more significantly compared with MICT.

CONCLUSIONS: HIIT was superior to MICT in improving depression in the PSD rats might via increasing mBDNF/proBDNF ratio and further improving neural plasticity in the hippocampus.