Journal of integrative neuroscience · 2025
The Crucial Role of Cerebellar Crus I in Electroacupuncture Pretreatment for Attenuating Myocardial Ischemia-Reperfusion Injury.
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Wu Yan, Shao Wen-Jing, Chang Hui-Min, Shu Qi, Zhou Xiang, Zhang Bin, Hu Ling, Wei Nai-Xuan, Zhang Fan, Cai Rong-Lin, Yu Qing
Аннотация
BACKGROUND: Electroacupuncture pretreatment (EA-pre) has been shown to help reduce myocardial ischemia-reperfusion injury (MIRI), but the underlying mechanism remains unclear. Our previous studies indicated that EA activates the cerebellar cortex, specifically the Crus Ⅰ. However, whether activation of the Crus Ⅰ contributes to the attenuation of MIRI induced by EA-pre remains unclear. This study investigated the possible relationship between EA-induced relief of MIRI and the activation of Crus Ⅰ.
METHODS: Electrocardiogram recording, echocardiography, and cardiac histology staining were used to assess the heart's functional status. In vivo electrophysiological recordings, Fos-targeted recombination in active populations (Fos-TRAP) gene-labeling technology and chemogenetic viral modulation were used to explore the effects of Crus Ⅰ activation in EA-pre on MIRI.
RESULTS: In vivo electrophysiological recordings demonstrated that Crus Ⅰ plays a crucial role in EA-pre by modulating sympathetic activity to alleviate MIRI. Subsequent Fos-TRAP studies showed that EA stimulation primarily induces changes in the neuronal activity of Crus Ⅰ Purkinje cells (Crus ⅠPC). Chemogenetic viral manipulations further verified that EA-pre suppresses PC activity in MIRI.
CONCLUSION: EA-pre mitigated cardiac sympathetic nerve dysfunction during MIRI by regulating Crus ⅠPC activity.
METHODS: Electrocardiogram recording, echocardiography, and cardiac histology staining were used to assess the heart's functional status. In vivo electrophysiological recordings, Fos-targeted recombination in active populations (Fos-TRAP) gene-labeling technology and chemogenetic viral modulation were used to explore the effects of Crus Ⅰ activation in EA-pre on MIRI.
RESULTS: In vivo electrophysiological recordings demonstrated that Crus Ⅰ plays a crucial role in EA-pre by modulating sympathetic activity to alleviate MIRI. Subsequent Fos-TRAP studies showed that EA stimulation primarily induces changes in the neuronal activity of Crus Ⅰ Purkinje cells (Crus ⅠPC). Chemogenetic viral manipulations further verified that EA-pre suppresses PC activity in MIRI.
CONCLUSION: EA-pre mitigated cardiac sympathetic nerve dysfunction during MIRI by regulating Crus ⅠPC activity.