Neuroprotectin/protectin D1 protects against neuropathic pain in mice after nerve trauma

Authors

  • Zhen-Zhong Xu PhD,

    1. Pain Signaling and Plasticity Laboratory, Department of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC
    2. Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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  • Xing-Jun Liu PhD,

    1. Pain Signaling and Plasticity Laboratory, Department of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC
    2. Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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  • Temugin Berta PhD,

    1. Pain Signaling and Plasticity Laboratory, Department of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC
    2. Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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  • Chul-Kyu Park PhD,

    1. Pain Signaling and Plasticity Laboratory, Department of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC
    2. Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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  • Ning Lü PhD,

    1. Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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  • Charles N. Serhan PhD,

    1. Center for Experimental Therapeutics and Reperfusion Injury, Harvard Institutes of Medicine and Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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  • Ru-Rong Ji PhD

    Corresponding author
    1. Pain Signaling and Plasticity Laboratory, Department of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC
    2. Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
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Abstract

Prevalence of neuropathic pain is high after major surgery. However, effective treatment for preventing neuropathic pain is lacking. Here we report that perisurgical treatment of neuroprotectin D1/protectin D1 (NPD1/PD1), derived from docosahexaenoic acid, prevents nerve injury-induced mechanical allodynia and ongoing pain in mice. Intrathecal post-treatment of NPD1/PD1 also effectively reduces established neuropathic pain and produces no apparent signs of analgesic tolerance. Mechanistically, NPD1/PD1 treatment blocks nerve injury-induced long-term potentiation, glial reaction, and inflammatory responses, and reverses synaptic plasticity in the spinal cord. Thus, NPD1/PD1 and related mimetics might serve as a new class of analgesics for preventing and treating neuropathic pain. Ann Neurol 2013;74:490–495

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