• Zhen-Zhong Xu, Xing-Jun Liu, Temugin Berta, Chul-Kyu Park, Ning Lü, Charles N Serhan, and Ru-Rong Ji.
• Pain Signaling and Plasticity Laboratory, Department of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC; Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
• Ann. Neurol. 2013 Sep 1;74(3):490-5.

AbstractPrevalence 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.Copyright © 2013 American Neurological Association.

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