Glycogen Synthase Kinase-3β Contributes to Remifentanil-Induced Postoperative Hyperalgesia via Regulating N-Methyl-D-Aspartate Receptor Trafficking

Abstract

The above results suggest that activation of GSK-3β contributes to remifentanil-induced postoperative hyperalgesia via regulating NMDA receptor subunits (NR1 and NR2B) trafficking in the spinal cord. Inhibition of GSK-3β may be an effective novel option for the treatment of remifentanil-induced postoperative hyperalgesia.