Electroacupuncture Enhances Cognitive Deficits in a Rat Model of Rapid Eye Movement Sleep Deprivation via Targeting MiR-132

Li Hao; Yiming Wu; Jin Xie; Xinwang Chen

doi:10.1155/2022/7044208

Electroacupuncture Enhances Cognitive Deficits in a Rat Model of Rapid Eye Movement Sleep Deprivation via Targeting MiR-132

Evid Based Complement Alternat Med. 2022 Sep 16:2022:7044208. doi: 10.1155/2022/7044208. eCollection 2022.

Authors

Li Hao¹, Yiming Wu², Jin Xie², Xinwang Chen²

Affiliations

¹ Medical College, Henan University of Chinese Medicine, Zhengzhou 450046, Henan, China.
² College of Acupuncture-Moxibustion and Tuina, Henan University of Chinese Medicine, Zhengzhou 450004, Henan, China.

Abstract

Deprivation of rapid eye movement sleep (REMSD) reduces the potential for learning and memory. The neuronal foundation of cognitive performance is synapse plasticity. MicroRNA-132 (MiR-132) is an important microRNA related to cognitive and synapse plasticity. Acupuncture is effective at improving cognitive impairment caused by sleep deprivation. Furthermore, its underlying principle is still unclear. Herein, whether electroacupuncture (EA) helps alleviate cognitive impairment in REMSD by targeting miR-132 was assessed. A rat model of REMSD was constructed using the developing multiplatform water environment technique, as well as EA therapy in Baihui (GV20) and Dazhui (GV14) was performed for 15 minutes, once daily for 7 days. Agomir or antagomir of MiR-132 was injected into the hippocampal CA1 areas to assess the EA mechanism in rats with REMSD. Then, the learning and memory abilities were detected by behavioral tests; synapse structure was assessed by transmission electron microscope (TCM); and dendrites branches and length were examined by Golgi staining. MiR-132-3p was assessed by real-time quantitative polymerase chain reaction (qRT-PCR). P250GAP, ras-related C3 botulinum toxin substrate 1 (Rac1), and cell division cycle 42 (Cdc42) expression levels in hippocampal tissues were evaluated by immunohistochemistry and Western blot. According to the research, EA therapy enhanced cognitive in REMSD rats, as evidenced by reduced escape latency; upregulated the performance of platform crossings and prolonged duration in the goal region; and improved spontaneous alternation. EA administration restored synaptic and dendritic structural damage in hippocampal neurons, enhanced miR-132 expression, and reduced p250GAP mRNA and protein levels. Additionally, EA boosted the protein level of Rac1 and Cdc42 associated with synaptic plasticity. MiR-132 agomir enhanced this effect, whereas miR-13 antagomir reversed this action. The current data demonstrate that EA at GV20 and GV14 attenuates cognitive impairment and modulates synaptic plasticity in hippocampal neurons via miR-132 in a sleep-deprived rat model.