Contralateral electroacupuncture modulates the transmission of nociceptive information in the spinal dorsal horn via GABAergic neurons in the rostral ventromedial medulla.
Kailing Zhang, Qingquan Yu, Yang Yang, He Zhu, Lingling Yu, Zhiyun Zhang, Kexing Wan, Jiajia Huang, Ping Peng, Jiwei Yao, Xianghong Jing, Man Li
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引用次数: 0
Abstract
Recent studies have shown that electroacupuncture (EA) can exert analgesic effects by modulating wide dynamic range (WDR) neurons in the spinal dorsal horn; however, how EA regulates WDR neurons to inhibit pain signals remains unclear. In this study, we identified a key brain region, rostral ventromedial medulla (RVM), involved in the modulation of spinal WDR neurons. Subsequently, we found evidence suggesting that GABAergic neurons in the RVM may mediate the transmission of nociceptive and non-nociceptive signals from the spinal cord, which underlies EA analgesia. The results demonstrated that the activation of RVM GABAergic neurons enhanced the excitability of WDR neurons, thereby facilitating the transmission of peripheral sensory signals within the spinal cord. Contralateral EA at 2 mA effectively suppressed WDR neuron activity and elevated pain thresholds in rats modeled with complete Freund's adjuvant (CFA). Notably, heightened activity of RVM GABAergic neurons mitigated the inhibitory effects of EA on WDR neurons and reduced EA-induced analgesia. These findings suggest that EA may attenuate WDR neuronal activity by modulating RVM GABAergic neurons, thereby inhibiting nociceptive transmission. This study highlights the potential involvement of RVM GABAergic neurons and identifies the efficacy of high-intensity, contralateral EA stimulation in producing analgesia.
期刊介绍:
Molecular Pain is a peer-reviewed, open access journal that considers manuscripts in pain research at the cellular, subcellular and molecular levels. Molecular Pain provides a forum for molecular pain scientists to communicate their research findings in a targeted manner to others in this important and growing field.