Publication details
Bilateral changes of SDF-1 and its receptor CXCR4 in the dorsal root ganglia of chronic constriction injury and spinal nerve ligation models of neuropathic pain
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| Year of publication | 2007 |
| Type | Appeared in Conference without Proceedings |
| MU Faculty or unit | |
| Citation | |
| Description | There is compelling evidence indicating that hyperalgesia, allodynia and ongoing pain associated with peripheral nerve injury are due to changes in the DRG. Chronic constriction injury (CCI) and spinal nerve ligation (SNL) are most frequently used experimental models of neuropathic pain based on nerve injury. Chemokines are small chemotactic cytokines which produce their effects by activating a family of G-protein coupled receptors. Some recent studies have shown that regulation of chemokines is one of the mechanisms underlying the development and maintenance of neuropathic pain. The biological activity of stromal cell-derived factor (SDF1) is signaled through the chemokine receptor CXCR4 which is unique among chemokine receptors, having only one known ligand. The role of SDF1/CXCR4 in the peripheral nervous system is implied by their early expression in neural crest cells/derivatives as well as in the dorsal root ganglia (DRG). The goal of our experiments was to compare an immunohistochemical staining for SDF-1 and CXCR4 proteins in the L4-L5 DRG of naive rats and those operated for unilateral L4-L5 SNL and CCI of sciatic nerve. The naive DRG displayed a sharp immunofluorescence for SDF1 (SDF1-IF) at the surface of neuron/satellite glial cell units. A significant decrease of SDF1-IF was induced bilaterally in the L4-L5 DRG 3 days after both CCI and SNL. A diffuse immunofluorescence for SDF1 was found in SGC after both types of nerve injuries for 1 and 2 weeks with a higher intensity following CCI. CXCR4-IF was present in the small- and medium sized neurons and the satellite glial cells (SGC) enveloping the large-sized neurons of naive DRG. CXCR4-IF was unchanged in the small- and medium sized neurons in the DRG from operated rats for all periods of survival. A significant reduced CXCR4-IF was observed in the SGC of contralateral DRG after both types of nerve injuries, but was elevated at the surface of large-sized neurons of ipsilateral DRG when CCI was applied. Latter pattern of staining was not significantly developed following SNL. Our results suggest different regulation of SDF1/CXCR4 expression in the DRG during various periods of survival and by the type of nerve injury used in neuropathic pain models. |
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