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Role of mitochondrial Ca 2+ uniporter in remifentanil-induced postoperative allodynia.

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  • معلومة اضافية
    • المصدر:
      Publisher: Wiley-Blackwell Country of Publication: France NLM ID: 8918110 Publication Model: Print Cited Medium: Internet ISSN: 1460-9568 (Electronic) Linking ISSN: 0953816X NLM ISO Abbreviation: Eur J Neurosci Subsets: MEDLINE
    • بيانات النشر:
      Publication: : Oxford : Wiley-Blackwell
      Original Publication: Oxford, UK : Published on behalf of the European Neuroscience Association by Oxford University Press, c1989-
    • الموضوع:
      Calcium/*metabolism ; Hyperalgesia/*drug therapy ; Mitochondria/*drug effects ; Remifentanil/*pharmacology; Analgesics, Opioid/pharmacology ; Animals ; Male ; Mitochondria/metabolism ; Phosphorylation ; Piperidines/pharmacology ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/drug effects ; Receptors, N-Methyl-D-Aspartate/metabolism ; Spinal Cord/drug effects ; Spinal Cord/metabolism
    • نبذة مختصرة :
      Opioid-induced hyperalgesia (OIH) and allodynia is a well-known phenomenon and refers to the pain sensitization in patients after prolonged opioid exposure. OIH limits the use of opioids in pain control, but the underlying mechanisms are not fully clear. This study investigated the role of mitochondrial Ca 2+ uniporter (MCU) in remifentanil (a commonly used opioid analgesic)-induced allodynia. Using a rat model of OIH, we found that incision- and remifentanil-induced mechanical allodynia were remarkably attenuated by pretreatment with Ru360, a specific MCU antagonist, suggesting a critical role of MCU in both incision- and opioid-induced allodynia. In addition, imaging studies with Rhod-2 (a mitochondrial Ca 2+ dye) in spinal tissues demonstrated increased mitochondrial Ca 2+ level in response to incision and remifentanil infusion, which was attenuated by Ru360. Western blot and immunohistochemistry showed that pNR [phosphorylated N-methyl-D-aspartate (NMDA) receptor] and pERK (phosphorylated extracellular signal-regulated kinase) are increased during both incision-induced hyperalgesia and remifentanil-induced hyperalgesia, and again the increases in pNR and pERK were remarkably attenuated by Ru360. Together, our data demonstrate that MCU plays a critical role in remifentanil-induced postoperative mechanical allodynia, with NMDA receptor and ERK as possible downstream effectors. Our findings provide novel mechanisms for remifentanil-induced mechanical allodynia and encourage future studies to examine the mitochondrial Ca 2+ uniporter as a potential therapeutic target for prevention of OIH.
      (© 2018 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)
    • Contributed Indexing:
      Keywords: NMDA receptor; extracellular signal-regulated protein kinase; opioid-induced hyperalgesia; rats
    • الرقم المعرف:
      0 (Analgesics, Opioid)
      0 (Piperidines)
      0 (Receptors, N-Methyl-D-Aspartate)
      P10582JYYK (Remifentanil)
      SY7Q814VUP (Calcium)
    • الموضوع:
      Date Created: 20180125 Date Completed: 20191029 Latest Revision: 20191029
    • الموضوع:
      20250114
    • الرقم المعرف:
      10.1111/ejn.13842
    • الرقم المعرف:
      29363836