Activation of the phosphoinositide 3-Kinase - Akt/PKB signaling pathway in primary sensory neurons after peripheral inflammation contributes to inflammatory mechanical hyperalgesia

Abstract

Phosphoinositide 3-Kinase (PI3K) is a lipid kinase that phophorylates the D-3 position of phosphatidylinositol lipids to produce PI(3,4,5)P3, which acts as a membrane-embedded secondary messenger to recruit and activate Akt/PKB. Current studies indicate that PI3K is involved in NGF-induced TRPV1 expression and sensitization, and mediates inflammatory heat hyperalgesia. In this study, we investigated whether the PI3K-Akt/PKB signaling pathway in primary sensory neurons is activated after peripheral inflammation and contributes to inflammatory mechanical hyperalgesia.