Xu, Bing, Guan, Xue-Hai, Yu, Jun-Xiong, Lv, Jing, Zhang, Helen, Fu, Qiao-Chu, Xiang, Hong-Bing, Bu, Hui-Lian, Shi, Dai, Shu, Bin, Qin, Li-Sheng, Manyande, Anne and Tian, Yu-Ke (2014) Activation of spinal phosphatidylinositol 3-kinase/protein kinase B mediates pain behavior induced by plantar incision in mice. Experimental Neurology, 255. pp. 71-82. ISSN 0014-4886Full text not available from this repository.
The 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.
|Uncontrolled Keywords:||phosphatidylinositol 3-kinase; protein kinase B; incisional pain; fos; center sensitization|
|Depositing User:||Anne Manyande|
|Date Deposited:||26 Oct 2015 15:26|
|Last Modified:||01 Jul 2016 13:52|
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