Electroacupuncture pretreatment ameliorates sleep deprivation-induced cardiac dysfunction via the regulation of GABAergic neuron activity in the cerebellar fastigial nucleus.

OBJECTIVE: Sleep deprivation (SD) is increasingly prevalent and associated with impaired cardiac function. Diminished γ-aminobutyric acid (GABA)-ergic neuronal activity in the cerebellar fastigial nucleus (FN) constitutes a key mechanism driving this disorder. Although electroacupuncture (EA) preconditioning has shown potential for mitigating SD-induced cardiac impairment, the underlying mechanisms remain unclear. Additionally, while it is known that FNGABA neurons contribute to the structural and functional integrity of cardiac autonomic regulation, the effects of EA on these neurons, specifically on their activity, have not been investigated. The objective of this study was to determine whether EA promotes cardiac function recovery by modulating FNGABA neuronal activity and to elucidate the neural-level mechanisms involved.

METHODS: To evaluate the effects of EA on SD, a mouse model of this condition was established. The mice were randomly divided into four groups: control, SD, sham EA + SD, and EA + SD. The outcomes were assessed based on cardiac function as well as the firing frequency and calcium activity of the FNGABA neurons. Finally, chemogenetic inhibition of FNGABA neurons was performed to verify their key role in the cardioprotective effects of EA.

RESULTS: SD significantly suppressed FNGABA neuronal activity, as indicated by reduced firing frequency and decreased calcium activity. Furthermore, SD induced cardiac dysfunction and sympathetic overactivation, impairing cardiac autonomic regulation. Notably, EA reversed the SD-induced inhibition of FNGABA neurons, significantly restoring neuronal firing rates and calcium signals. Conversely, chemogenetic inhibition of FNGABA neurons abolished the cardioprotective effects of EA. Mechanistically, the preventive effects of EA against SD-induced cardiac injury were mediated via the modulation of FNGABA neuronal activity.

CONCLUSION: EA alleviates SD-induced cardiac dysfunction by restoring FNGABA neuronal activity. These findings indicate that EA protects against SD-related cardiac injury by modulating the activity of FNGABA neurons. Please cite this article as: Shao WJ, Liu W, Zhang F, Wu Y, Xu ZH, Luo ZJ, Peng QM, Wei NX, Xu NG, Yu Q, Cai RL. Electroacupuncture pretreatment ameliorates sleep deprivation-induced cardiac dysfunction via the regulation of GABAergic neuron activity in the cerebellar fastigial nucleus. J Integr Med. 2026; Epub ahead of print.