• Bing Xu, Xue-Hai Guan, Jun-Xiong Yu, Jing Lv, Hong-Xing Zhang, Qiao-Chu Fu, Hong-Bing Xiang, Hui-Lian Bu, Dai Shi, Bin Shu, Li-Sheng Qin, Anne Manyande, and Yu-Ke Tian.
• Department of Neurology, Liuzhou Traditional Chinese Medical Hospital, the Third Affiliated Hospital of Guangxi University of Chinese Medicine, 32 Jiefang West Road, Liuzhou 545001, PR China.
• Exp. Neurol. 2014 May 1; 255: 71-82.

AbstractThe etiology of postoperative pain may be different from antigen-induced inflammatory pain and neuropathic pain. However, central neural plasticity plays a key role in incision pain. It is also known that phosphatidylinositol 3-kinase (PI3K) and protein kinase B/Akt (PKB/Akt) are widely expressed in laminae I-IV of the spinal horn and play a critical role in spinal central sensitization. In the present study, we explored the role of PI3K and Akt in incision pain behaviors. Plantar incision induced a time-dependent activation of spinal PI3K-p110γ and Akt, while activated Akt and PI3K-p110γ were localized in spinal neurons or microglias, but not in astrocytes. Pre-treatment with PI3K inhibitors, wortmannin or LY294002 prevented the activation of Akt brought on by plantar incision in a dose-dependent manner. In addition, inhibition of spinal PI3K signaling pathway prevented pain behaviors (dose-dependent) and spinal Fos protein expression caused by plantar incision. These data demonstrated that PI3K signaling mediated pain behaviors caused by plantar incision in mice. Copyright © 2014 Elsevier Inc. All rights reserved.

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