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VEGF and its receptor-2 involved in neuropathic pain transmission mediated by P2X2/3receptor of primary sensory neurons

Authors
Journal
Brain Research Bulletin
0361-9230
Publisher
Elsevier
Publication Date
Volume
83
Issue
5
Identifiers
DOI: 10.1016/j.brainresbull.2010.08.002
Keywords
  • Vegf
  • Vegf Receptor-2
  • P2X2/3Receptor
  • Neuropathic Pain
  • Primary Sensory Neuron
Disciplines
  • Chemistry

Abstract

Abstract The pathogenesis of neuropathic pain is complex. P2X 2/3 receptor plays a crucial role in nociception transduction of chronic pain. VEGF inhibitors are effective for pain relief. The present study investigated the effects of VEGF and VEGF receptor-2 (VEGFR2) on the pain transmission in neuropathic pain states that mediated by P2X 2/3 receptor in primary sensory neurons. Chronic constriction injury (CCI) model was used as neuropathic pain model. Sprague–Dawley rats had been randomly divided into sham group, CCI group and CCI rats treated with anti-rVEGF antibody group. Mechanical withdrawal threshold and thermal withdrawal latency were measured. Expressions of VEGF, VEGFR2 and P2X 2/3 in L4–6 dorsal root ganglia (DRG) were detected by immunohistochemistry, RT-PCR and western blot analysis. The mechanical withdrawal threshold and thermal withdrawal latency in CCI group were lower than those in sham group and CCI rats treated with anti-rVEGF antibody group ( p < 0.05), while VEGF, VEGFR2 and P2X 2/3 receptors’ expressions of L4–6 DRG in CCI group were higher than those in the other two groups ( p < 0.05). The expressions of VEGF, VEGFR2 and P2X 2/3 in L4–6 DRG of CCI rats treated with anti-rVEGF antibody group were decreased compared with those in CCI group ( p < 0.05). The results show that VEGF and VEGFR2 are involved in the pathogenesis of neuropathic pain and VEGF primarily potentiates pain responses mediated by P2X 2/3 receptor on DRG neurons. Anti-rVEGF treatment in CCI rats may alleviate chronic neuropathic pain by decreasing the expressions of VEGFR2 and P2X 2/3 receptors on DRG neurons to inhibit the transmission of neuropathic pain signaling.

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