Figure 2.

Modeling signaling events elicited by PGE2 before and after inflammation. Activation of EP receptors by PGE2 promotes cAMP synthesis. Under normal conditions (blue), cAMP activates PKA and enhances the activity of P2X3Rs. After inflammation (red), cAMP also activates Epacs which leads to the activation of PKCɛ and PKCα to give rise to much enhanced P2X3R-mediated responses and exaggerated primed hyperalgesia.

PGE2: prostaglandin E2; AC: adenylyl cyclase; ATP: adenosine triphosphate; cAMP: cyclic adenosine 3′,5′-monophosphate; Epac: exchange protein activated by cAMP; PKA: protein kinase A; PKC: protein kinase C.