Receptor for Activated C Kinase 1 Mediates the Chronic Constriction Injury-induced Neuropathic Pain in the Rats’ Peripheral and Central Nervous System

In this study, the biological effects and mechanisms of RACK1 contributes to the pathogenesis of chronic constriction injury (CCI)-induced neuropathic pain were investigated. By western blot and staining, we found that RACK1 protein changed in dorsal root ganglion (DRG) neurons and spinal cord (SC) neurons except glial cells after CCI. Especially, RACK1 was co-located with IB4-, CGRP-positive neurons, suggesting it was related to integrate nociceptive information from the primary afferents in DRG. The successful establishment of CCI models also directly led to mechanical allodynia and heat hyperalgesia, which could be reversed by intrathecal injection of RACK1 siRNA. Furthermore, intrathecal injection of RACK1 siRNA reduced the expression of RACK1 and accompanying spinal c-fos, which is the transcription factor and marker of neuronal activation. These results suggested that targeting RACK1 be a sensible approach for treating NP.
Source: Neuroscience Letters - Category: Neuroscience Source Type: research