Electroacupuncture at combined acupoints GV20/ST36/GB34 regulates BDNF/TrkB-mediated synaptic remodeling and alleviates post-stroke sensorimotor deficits in male rats.

OBJECTIVE: This study investigated whether electroacupuncture (EA) at combined acupoints GV20/ST36/GB34 improves post‑stroke sensorimotor deficits in male rats, with a focus on synaptic plasticity and glial cell‑mediated neuroinflammation. METHODS: A transient right middle cerebral artery occlusion (MCAO) stroke model was successfully established in 47 SPF male SD rats. The rats were divided into the MCAO group (n = 11), the Sham-EA group (acupuncture at GV20/ST36/GB34 only, n = 12), the EA group (EA at GV20/ST36/GB34, n = 12), and the EA+ANA-12 group (stereotactic injection of ANA-12 in addition to EA, n = 12). Additionally, 12 SPF male SD rats were included in the Sham group (without MCAO). Sensorimotor functions were assessed by behavioral tests. Cerebral infarction, neuronal damage, microglial activation, and synaptic protein expression were evaluated using TTC staining, Nissl staining, immunofluorescence, and immunohistochemistry. BDNF/TrkB pathway expression and inflammatory markers were detected by RT‑qPCR, Western blot, and ELISA. RESULTS: EA at GV20/ST36/GB34 improved these deficits, promoted synaptic remodeling, suppressed microglial activation, and reduced neuroinflammation, accompanied by activation of the BDNF/TrkB pathway. Notably, the protective effects of EA were partially reversed by ANA‑12, indicating that BDNF/TrkB signaling is a key, but not the exclusive, mediator of EA's therapeutic effects. CONCLUSION: EA at combined acupoints GV20/ST36/GB34 alleviates post‑stroke sensorimotor deficits in male rats by promoting synaptic plasticity and mitigating neuroinflammation, partially through the BDNF/TrkB pathway.