Effect of CXCL12/CXCR4 signaling on neuropathic pain after chronic compression of dorsal root ganglion

Neuropathic pain is a complex, chronic pain state that often accompanies tissue damage, inflammation or injury of the nervous system. However the underlying molecular mechanisms still remain unclear. Here, we showed that CXCL12 and CXCR4 were upregulated in the dorsal root ganglion (DRG) after chron...

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Bibliographic Details
Published in:Scientific reports 2017-07, Vol.7 (1), p.5707-11, Article 5707
Main Authors: Yu, Yang, Huang, Xini, Di, Yuwei, Qu, Lintao, Fan, Ni
Format: Article
Language:English
Subjects:
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Animals
Calcitonin gene-related peptide
Calcium
Capsaicin receptors
Cells, Cultured
Chemokine CXCL12 - metabolism
Chronic pain
Compression
CXCL12 protein
CXCR4 protein
Depolarization
Dorsal root ganglia
Ganglia, Spinal - physiopathology
Heterocyclic Compounds - pharmacology
Humanities and Social Sciences
Hyperalgesia - physiopathology
Membrane potential
Membrane Potentials - physiology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Molecular modelling
multidisciplinary
Nervous system
Neuralgia
Neuralgia - physiopathology
Neurons, Afferent - physiology
Pain
Pain Measurement
Pain perception
Receptors, CXCR4 - metabolism
Rodents
Science
Science (multidisciplinary)
Sensory neurons
Signal Transduction
Substance P
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Description
Summary:Neuropathic pain is a complex, chronic pain state that often accompanies tissue damage, inflammation or injury of the nervous system. However the underlying molecular mechanisms still remain unclear. Here, we showed that CXCL12 and CXCR4 were upregulated in the dorsal root ganglion (DRG) after chronic compression of DRG (CCD), and some CXCR4 immunopositive neurons were also immunopositive for the nociceptive neuronal markers IB4, TRPV1, CGRP, and substance P. The incidence and amplitude of CXCL12-induced Ca 2+ response in primary sensory neurons from CCD mice was significantly increased compared to those from control animals. CXCL12 depolarized the resting membrane potential, decreased the rheobase, and increased the number of action potentials evoked by a depolarizing current at 2X rheobase in neurons from CCD mice. The mechanical and thermal hypernociception after CCD was attenuated by administration of a CXCR4 antagonist AMD3100. These findings suggest that CXCL12/CXCR4 signaling contributes to hypernociception after CCD, and targeting CXCL12/CXCR4 signaling pathway may alleviate neuropathic pain.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-017-05954-1