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Article

Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain

  • Authors:
    • Xu‑Dan Shi
    • Di Fu
    • Jun‑Mei Xu
    • Yan‑Ling Zhang
    • Ru‑Ping Dai
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesia, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China, Department of Anesthesia, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China
  • Pages: 1661-1665
    |
    Published online on: February 28, 2013
       https://doi.org/10.3892/mmr.2013.1347
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Abstract

Extracellular signal‑regulated kinase (ERK) 1/2 in the spinal cord has been implicated in the development of neuropathic pain and inflammatory pain. However, a limited number of studies have investigated the role of spinal ERK in incisional pain. The present study aimed to determine the role of ERK in the spinal cord in incisional pain. Incisional pain was established in rats by a unilateral hind paw incision. ERK1/2 expression was analyzed by immunohistochemistry. Hypersensitivity to pain was evaluated by measuring the paw withdrawal threshold using the von Frey test. The mitogen‑activated protein kinase kinase (MEK) inhibitor, U0126, was administered 20 min prior to or 10 min following the incision by intrathecal or intraperitoneal injection. Phosphorylated ERK1/2 in the ipsilateral L4‑5 spinal superficial dorsal horn was activated 1 min following the incision, reached its peak level at 5 min and then returned to the basal level 20 min following the incision. Pretreatment, but not post‑treatment with U0126 markedly attenuated the pain hypersensitivity induced by the incision. Therefore, the present study indicates that the transient activation of spinal ERK1/2 contributes to the initiation of pain hypersensitivity following surgical incision.
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Copy and paste a formatted citation
Spandidos Publications style
Shi XD, Fu D, Xu JM, Zhang YL and Dai RP: Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain. Mol Med Rep 7: 1661-1665, 2013.
APA
Shi, X., Fu, D., Xu, J., Zhang, Y., & Dai, R. (2013). Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain. Molecular Medicine Reports, 7, 1661-1665. https://doi.org/10.3892/mmr.2013.1347
MLA
Shi, X., Fu, D., Xu, J., Zhang, Y., Dai, R."Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain". Molecular Medicine Reports 7.5 (2013): 1661-1665.
Chicago
Shi, X., Fu, D., Xu, J., Zhang, Y., Dai, R."Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain". Molecular Medicine Reports 7, no. 5 (2013): 1661-1665. https://doi.org/10.3892/mmr.2013.1347
Copy and paste a formatted citation
x
Spandidos Publications style
Shi XD, Fu D, Xu JM, Zhang YL and Dai RP: Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain. Mol Med Rep 7: 1661-1665, 2013.
APA
Shi, X., Fu, D., Xu, J., Zhang, Y., & Dai, R. (2013). Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain. Molecular Medicine Reports, 7, 1661-1665. https://doi.org/10.3892/mmr.2013.1347
MLA
Shi, X., Fu, D., Xu, J., Zhang, Y., Dai, R."Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain". Molecular Medicine Reports 7.5 (2013): 1661-1665.
Chicago
Shi, X., Fu, D., Xu, J., Zhang, Y., Dai, R."Activation of spinal ERK1/2 contributes to mechanical allodynia in a rat model of postoperative pain". Molecular Medicine Reports 7, no. 5 (2013): 1661-1665. https://doi.org/10.3892/mmr.2013.1347
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