• Neuroscience · Feb 2025

    NRG1-ErbB4 signaling in the cerebrospinal fluid-contacting nucleus regulates thermal pain in mice.

    • Yuhan Ding, Yao Yan, Wei Song, Ying Li, Jing Zhao, Bin Gui, Yijun Zhang, and Licai Zhang.
    • Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, China; Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou Medical University, Xuzhou, China; NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Xuzhou, China.
    • Neuroscience. 2025 Feb 6; 566: 132141132-141.

    AbstractThe cerebrospinal fluid-contacting nucleus(CSF-contacting nucleus) is a pair of unique nuclei in the brain parenchyma which has long been demonstrated to play an important role in pain signal processing. However, the mechanisms by which the CSF-contacting nucleus intervenes in pain is unclear. The NRG1-ErbB4 signaling plays an important role in the nervous system and has been shown to be involved in the regulation of pain. Whether there is an involvement of NRG1-ErbB4 signaling in the regulation of pain in the CSF-contacting nucleus is currently unknown. Here, our works showed that c-Fos expression in the CSF-contacting nucleus was increased in response to incisional pain. The activation of the CSF-contacting nucleus by chemogenetics could induce thermal hyperalgesia in naive mice without effecting the pain in mice suffering from incision pain. The inhibition of the CSF-contacting nucleus alleviated incision pain, but had no effect on the pain response in naive mice. With immunofluorescence staining and Western blot, the NRG1-ErbB4 signaling in the CSF-contacting nucleus showed upregulated during the acute pain phase. And, activating NRG1-ErbB4 signaling in the CSF-contacting nucleus specifically by intracranial injection of drugs, the naïve mice displayed thermal hyperalgesia while inhibiting this signaling by intracranial injection could reverse the hyperalgesia caused by CSF-contacting nucleus activation, and execute an analgesic effect during the painful phase in mice. Our study suggested that the CSF-contacting nucleus plays a regulatory role in thermal pain in mice via NRG1-ErbB4 signaling.Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

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