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Figure 5 | Molecular Pain

Figure 5

From: Carrageenan induced phosphorylation of Akt is dependent on neurokinin-1 expressing neurons in the superficial dorsal horn

Figure 5

Schematic of hypothesis: Inflammation induced release of spinal TNF activates PI-3K probably via TNF receptor 1. PI-3K leads to phosphorylation of Akt, both directly and indirectly through PDK1. P-Akt activates signal transduction cascades leading to central sensitization. PDK1 also activates PKA, which phosphorylates GluA1 at ser 845. Phosphorylation at this site lowers the energy required for GluA1 insertion into the plasma membrane as part of a functional AMPA receptor. Increased AMPA receptor density, especially AMPA receptors enriched with GluA1 rather than GluA2, contributes to spinal long term potentiation and pain behavior. Despite the fact that they both are initiated through a PI-3K linkage, phosphorylation of Akt and GluA1 trafficking seem to be independent of one another.

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Molecular Pain

ISSN: 1744-8069

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