| Summary: | Neurotrophins, such as brain-derived neurotrophic factor (BDNF), have shown promise as neuroprotective agents, indicating their potential in therapeutic strategies for neurodegenerative disease. However, the inherent bioactivity and pharmaceutical limitations of BDNF compromise its clinical efficacy. Research has documented the beneficial effects of electroacupuncture (EA) against neurodegeneration, possibly by BDNF-mediated mechanisms. The present study was designed to clarify whether EA can mount a neuroprotective effect in mice lesioned with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) via stimulation of the BDNF-TrkB signaling pathway. We found that EA not only ameliorated the motor dysfunction but also restored the dopaminergic neuronal function and upregulated BDNF expression in MPTP-lesioned mice. Interestingly, the TrkB inhibitor K252a abolished the neuroprotective effects of EA. Western blot analyses further demonstrated that EA might recover the level of phospho-Akt, phospho-ERK1/2, and BDNF against MPTP neurotoxicity via reversing the imbalance between TrkB FL and TrkB T1. Taken together, the results of the present study show that EA stimulation can ameliorate MPTP-induced parkinsonism in mice. Such a neuroprotective effect may be partially mediated via restoring TrkB neurotrophic signaling.
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