CBP Expression Contributes to Neuropathic Pain via CREB and MeCP2 Regulation in the Spared Nerve Injury Rat Model

This study investigates how neuropathic pain, a type of chronic pain caused by nerve damage, is related to two proteins: CREB-binding protein (CBP) and methyl-CpG-binding protein 2 (MeCP2). These proteins are involved in epigenetic regulation, which can change how genes are expressed without altering the DNA sequence. The researchers used a rat model of spared nerve injury (SNI) to mimic nerve damage. They examined the levels of CBP and MeCP2 in the spinal cord and dorsal root ganglion (DRG), which are important for pain signaling. They also tested whether blocking CBP or MeCP2 could reduce pain. The results suggest that CBP and MeCP2 play a role in the development of neuropathic pain after nerve injury. Specifically, CBP appears to be involved in both the development and maintenance of this pain, while the role of MeCP2 may be more complex and requires further study.

• 1
  SNI induced a significant increase in the number of CBPs in the L4 dorsal horn of the spinal cord compared to control groups, indicating an upregulation of CBP expression after nerve injury.
• 2
  The number of MeCP2 cells in the dorsal horn on the ipsilateral side decreased significantly compared with the contralateral dorsal horn and the control group, suggesting a downregulation of MeCP2 expression.
• 3
  Blocking CBP with siRNA significantly reduced mechanical allodynia (pain from non-painful touch) in the SNI model, suggesting that CBP contributes to the development and maintenance of neuropathic pain.