LAUSR

Studies have shown that electroacupuncture (EA) can effectively improve vascular cognitive impairment (VCI), but its mechanisms have not been clearly elucidated. This study is aimed at investigating the mechanisms underlying the effects of EA treatment on hippocampal synaptic transmission efficiency and plasticity in rats with VCI. Methods. Sprague–Dawley rats were subjected to VCI with bilateral common carotid occlusion (2VO). EA stimulation was applied to Baihui (GV20) and Shenting (GV24) acupoints for 30 min once a day, five times a week, for four weeks. Our study also included nonacupoint groups to confirm the specificity of EA therapy. The Morris water maze (MWM) was used to assess cognitive function. Electrophysiological techniques were used to detect the field characteristics of the hippocampal CA3–CA1 circuit in each group of rats, including input-output (I/O), paired-pulse facilitation ratios (PPR), field excitatory postsynaptic potential (fEPSP), and excitatory postsynaptic current (EPSC). The expression of synapse- and calcium-mediated signal transduction associated proteins was detected through western blotting. Results. The MWM behavioural results showed that EA significantly improved cognitive function in VCI model rats. EA increased the I/O curve of VCI model rats from 20 to 90 μA. No significant differences were observed in hippocampal PPR. The fEPSP of the hippocampal CA3–CA1 circuit was significantly increased after EA treatment compared with that after nonacupuncture treatment. We found that EA led to an increase in the EPSC amplitude and frequency, especially in the decay and rise times. In addition, the protein expression and phosphorylation levels of N-methyl-D-aspartate receptor 2B, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor 1, and Ca2+-calmodulin-dependent protein kinase II increased to varying degrees in the hippocampus of VCI model rats. Conclusion. EA at GV20 and GV24 acupoints increased the basic synaptic transmission efficiency and synaptic plasticity of the hippocampal CA3–CA1 circuit, thereby improving learning and memory ability in rats with VCI.