The impact of N-cadherin-β-catenin signaling on the analgesic effects of glial cell-derived neurotrophic factor in neuropathic pain.

Abstract:

:Long-term neuropathic pain can lead to anxiety, depression, and other issues, which seriously affect patients' quality of life. For this reason, it is important to find effective treatments. Studies have shown that glial cell-derived neurotrophic factor (GDNF) can relieve neuropathic pain. However, its mechanism of action is unknown. Our previous study of GDNF suggested that the N-cadherin-β-catenin transmembrane signaling system might play a role in GDNF transmembrane signaling. Based on this, the current study aimed to produce a neuropathic pain model to confirm the activation of the N-cadherin-β-catenin signaling system in the spinal dorsal horn under pain conditions and to study the impact of GDNF intrathecal injection on central sensitization of dorsal horn neurons. The results showed that N-cadherin expression, as well as the expression of membrane-associated β-catenin, was reduced in the dorsal horn of the spinal cord in the chronic pain model. Intrathecal injection of GDNF could reactivate the N-cadherin-β-catenin system, improve central sensitization, and relieve pain. Knockdown of N-cadherin or β-catenin could significantly reduce the analgesic effect of GDNF. These results provide clear experimental evidence that the N-cadherin-β-catenin signaling system participates in the analgesic effect of GDNF in neuropathic pain and help identify transmembrane and intracellular signal transduction mechanisms associated with GDNF's analgesic effects.

authors

Pan Y,Jiang L,Wang C

doi

10.1016/j.bbrc.2019.11.076

subject

Has Abstract

pub_date

2020-02-05 00:00:00

pages

463-470

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)32196-5

journal_volume

522

pub_type

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