CXCR3 signalling partially contributes to the pathogenesis of neuropathic pain in male rodents. (10th October 2021)

• Record Type: Journal Article
• Authors: Li, Kai; Tan, Yong‐Hui; Feng, Shi‐Yang; Fu, Kai‐Yuan
• Other Names: Fu Kai‐Yuan guestEditor.; Wang Kelun guestEditor.; Wang Mei‐Qing guestEditor.; Cao Ye guestEditor.
• Is Part Of: Journal of oral rehabilitation. Volume 49:Number 2(2022)
• Page Start: 186
• Page End: 194
• Publication Date: 2021-10-10
• Subjects: chronic constriction injury (CCI) -- CXCR3 -- microglia -- neuropathic pain -- phosphorylated‐p38; Dentistry -- Periodicals; Prosthodontics -- Periodicals; 617
• DOI: 10.1111/joor.13262
• Languages: English
• ISSNs: 0305-182X

Abstract

Abstract: Background: Currently, there is a lack of effective therapy for chronic pain. Increasing evidence has shown that chemokines and their correlative receptors involved in the neuron–glial cell cross‐talk could contribute to the pathogenesis of neuropathic pain. Our previous studies suggested that CXCR3 expression was elevated in the spinal dorsal horn after nerve injury. Objectives: In this study, we aimed to explore the role of CXCR3 signalling in chronic pain modulation. Methods: Reverse transcription quantitative PCR and Western blotting were used to measure the expression of CXCR3 and its ligands in the spinal cord following chronic constriction injury (CCI) of the sciatic nerve. Cxcr3 ‐knockout mice were used to observe the effect of the receptor on pain‐related behaviour and microglial activation. Immunohistochemistry was used to investigate the expression of two activation markers for spinal microglia, Iba‐1 and phosphorylated‐p38 (p‐p38) in these mice. Results: The expression of CXCR3 and its ligand CXCL11 was upregulated in the lumbar dorsal horn of the spinal cord in CCI models. In Cxcr3 ‐knockout mice, CCI‐induced tactile allodynia and thermal hyperalgesia were observed to be alleviated during the early stage of pain processing. Meanwhile, the expression of the glial activation markers, namely, Iba‐1 and p‐p38, was decreased. Conclusion: Our results demonstrate that CXCR3 could be a key modulator involved in pain modulation of the spinal cord; therefore, CXCR3‐related signalling pathways could be potential targets for the treatment of intractable pathological pain. Abstract : CXCR3 and its ligand CXCL11 were upregulated in the spinal cord and partially contributed to nerve injury inducedhyperalgesia. CXCR3 signaling was involved in the pathogenesis of neuropathic pain in male rodents.