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Details

Autor(en) / Beteiligte
Titel
Activation of spinal phosphatidylinositol 3-kinase/protein kinase B mediates pain behavior induced by plantar incision in mice
Ist Teil von
  • Experimental neurology, 2014-05, Vol.255, p.71-82
Ort / Verlag
Amsterdam: Elsevier Inc
Erscheinungsjahr
2014
Quelle
MEDLINE
Beschreibungen/Notizen
  • 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. •Plantar incision induced a time-dependent activation of PI3K and Akt in spinal cord and dorsal root ganglion.•Inhibition of spinal PI3K prevented pain behaviors and spinal Fos expression induced by plantar incision.•Inhibition of spinal PI3K prevented Akt protein expression induced by plantar incision.

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