Fig. 5. Role of β-catenin system in induction of neuropathic pain.

In the physiological state, absence of Wnt leads to decreased levels of β-catenin in the cytoplasm as GSK-3b phosphorylates b-catenin and leads to its proteosomal degradation (A). During the nerve injury, Wnt binds to its receptor frizzled and suppresses the GSK-3β phosphorylation of β-catenin. Increased β-catenin binds to TCF4 and activates Wnt target genes that are responsible for neuropathic pain (B).