Electroacupuncture ameliorates sleep deprivation-induced insomnia in mice by regulating the dopaminergic projections from VTA to NAc

IF 4.6 2区医学 Q1 NEUROSCIENCES

Experimental Neurology Pub Date : 2025-06-17 DOI:10.1016/j.expneurol.2025.115351

Weichao Pan , Sijia Wang , Ying Liu , Shan Qin , Feifei Ge , Xiya Yuan , Yuyang Bo , Haoqing Tai , Chengyong Liu , Yu Fan , Xiaoqiu Wang , Hee Young Kim , Wenzhong Wu , Xiaowei Guan

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Abstract

Background

The electroacupuncture (EA) has emerged as a potential therapeutic approach for the treatment of chronic insomnia, however, its underlying brain mechanism remain unclear. Methods: Chronic sleep deprivation (CSD) mice models was established to investigate the effect of EA at acupoints of Yintang (EX-HN3), Shenmen (HT7), and Sanyinjiao (SP6) on CSD. With the methods of EEG/EMG recordings and chemogenetic manipulations, we explore the role of the dopaminergic projections from ventral tegmental area (VTA) to nucleus accumbens (NAc) in the therapeutic effects of EA on CSD-induced insomnia.

Results

We found that EA significantly alleviated CSD-induced insomnia, as indicated by an increased total sleep time and non-rapid eye movement (NREM) sleep during the dark period, along with attenuating the CSD-caused hyperactivity of VTA dopamine neurons in mice. Chemogenetic inhibition of the dopaminergic projections from VTA to NAc could restore the NREM sleep in CSD mice. Most importantly, the therapeutic effects of EA on CSD-induced insomnia was counteracted by activating the dopaminergic projections from VTA to NAc of mice.

Conclusion

These findings suggested that the therapeutic effects of EA at EX-HN3, HT7 and SP6 are achieved by targeting the dopaminergic projections from VTA to NAc, which could be therapeutic approach for chronic insomnia.

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电针通过调节VTA到NAc的多巴胺能投射来改善睡眠剥夺引起的小鼠失眠

电针（EA）已成为治疗慢性失眠的一种潜在的治疗方法，然而，其潜在的脑机制尚不清楚。方法：建立慢性睡眠剥夺（CSD）小鼠模型，观察电针穴位银堂（EX-HN3）、神门（HT7）、三阴角（SP6）对慢性睡眠剥夺的影响。采用脑电图/肌电图记录和化学发生手法，探讨了多巴胺能从腹侧被盖区（VTA）向伏隔核（NAc）的投射在EA治疗csd致失眠中的作用。结果我们发现，EA显著减轻了csd诱导的失眠，这表明，在黑暗时期，总睡眠时间和非快速眼动（NREM）睡眠时间增加，同时减弱了csd引起的小鼠VTA多巴胺神经元的过度活跃。化学发生抑制VTA向NAc的多巴胺能投射可恢复CSD小鼠NREM睡眠。最重要的是，EA对csd致失眠的治疗作用通过激活小鼠VTA到NAc的多巴胺能投射而被抵消。结论EA对EX-HN3、HT7和SP6的治疗作用是通过靶向VTA向NAc的多巴胺能投射而实现的，可能是治疗慢性失眠的一种途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Experimental Neurology 医学-神经科学

CiteScore

10.10

自引率

3.80%

发文量

258

审稿时长

42 days

期刊介绍： Experimental Neurology, a Journal of Neuroscience Research, publishes original research in neuroscience with a particular emphasis on novel findings in neural development, regeneration, plasticity and transplantation. The journal has focused on research concerning basic mechanisms underlying neurological disorders.