Electroacupuncture Increases the Hippocampal Synaptic Transmission Efficiency and Long-Term Plasticity to Improve Vascular Cognitive Impairment

Abstract

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.

The effects and mechanisms of acupuncture for post-stroke cognitive impairment: progress and prospects

“…The CaM-CaMKIV-CREB signaling pathway may play an important role in the regulation of PSCI by EA ( Zhang et al, 2016 ). EA at GV20 and GV24 can downregulate the protein expression and phosphorylation levels of NMDAR2B, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) and CaMKII in the hippocampus, enhance LTP, increased the basic synaptic transmission efficiency and synaptic plasticity of the hippocampal CA3-CA1 circuit, further improving learning and memory abilities in the 2VO-induced rats ( Dai et al, 2022 ). 3′, 5′-cyclic AMP (cAMP)/protein kinase A (PKA)/CREB has also been shown to be involved in the LTP process that mediates synaptic transmission.…”

Electroacupuncture Attenuates Neuropathic Pain in a Rat Model of Cervical Spondylotic Radiculopathy: Involvement of Spinal Cord Synaptic Plasticity

“… 52 , 53 Additionally, synaptic plasticity is the cellular physiological basis of pain signal transmission, including changes in synaptic structure and function. 54 Despite exploring the effects of EA on synaptic morphology structure, our study did not examine long-term potentiation using electrophysiological techniques, which will be assessed in our future studies.…”

The neuroprotective and neural circuit mechanisms of acupoint stimulation for cognitive impairment

“…Late-LTP involves the activation of 3′, 5′ cyclic adenosine monophosphate (cAMP) by activated CaMKII, regulating the protein kinase A (PKA)/CREB pathway and increasing the number of AMPAR [ 119 , 120 ]. EA increased the levels of CaMKII in the hippocampus [ 121 , 122 ] while acupuncture at ST36 alleviated disordered LTP in the perforant pathway-dentate gyrus (PP-DG), and counteracted decreases in cAMP, PKA, and p-CREB in cerebral multi-infarction rats. Increased CREB phosphorylation and the improvement in cognitive function were both blocked by the PKA inhibitor N- [2-(p-bromocinnamyl amino) ethyl] -5-isoquinoline-sulfonamide [ 123 ].…”