☆ 4.7 Article

Activation of spinal phosphatidylinositol 3-kinase/protein kinase B mediates pain behavior induced by plantar incision in mice

EXPERIMENTAL NEUROLOGY (2014)

期刊

EXPERIMENTAL NEUROLOGY

卷 255, 期 -, 页码 71-82

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE

DOI: 10.1016/j.expneurol.2014.02.019

关键词

Phosphatidylinositol 3-Idnase; Protein kinase B; Incisional pain; Fos; Center sensitization

类别

Neurosciences

资金

Guangxi Natural Science Foundation [2012GXNSFBA053123]
National Natural Science Foundation of China [81100832, 81371250, 81200862]

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Protocol

Reagent

摘要

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-p110 gamma and Akt, while activated Akt and PI3K-p1 10 gamma were localized in spinal neurons or microglias, but not in astrocytes. Pre-treatment with PI3K inhibitors, wortrnannin 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. (C) 2014 Elsevier Inc All rights reserved.

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