Abstract
A peripheral nerve injury induces cellular and molecular changes in the corresponding (homologous) DRG responsible for ectopic discharge of the primary sensory neurons, factor thought to contribute to the development and maintenance of neuropathic pain. Macrophages increase in number in corresponding DRG following nerve injury, and their activity is referred to be important in initiating of neuropathic pain. Sciatic nerve ligature and ventral root transection are used as experimental models of neuropathic pain with different mechanisms of effect to DRG. Macrophages exhibiting ED-1+ immunostaining were examined quantitatively in the rat L4-L5 DRG from both ipsi- and contralateral side following unilateral sciatic nerve ligature (SNL) or ventral root transection (VRT) under an aseptic condition. An amount of ED-1+ macrophages were found in the interstitial space of naive DRG without intimate location to the neuronal bodies. In comparison to naive DRG, area of ED-1+ cells was significantly enlarged in ipsilateral DRG 2 and 4 weeks from SNL. The ED-1+ macrophages and their cytoplasmic processes were frequently located close to neuronal bodies to become their satellite cells. Contralateral DRG also displayed an increased amount of ED-1+ macrophages, but significant enlargement was found only following 4 weeks when compared with naive DRG or contralateral DRG after 2 weeks. In all cases, contralateral in contrast to ipsilateral DRG contained significantly lower amount of ED-1+ cells. Ventral root transection for 2 and 4 weeks resulted in an increased amount of ED1+ cells in both ipsi- and contralateral DRG in comparison to naive ones. However, the enlargement was similar on both sides after 2 weeks, but greater elevation was observed only in ipsilateral DRG 4 weeks from VRT. The results indicate that SNL stimulated invasion of ED1+ macrophages predominantly into ipsilateral DRG, and later (4 weeks) to contralateral ones. In contrast, VRT induced a higher invasion of ED1+ cells to contralateral DRG already after 2 weeks. Our results suggested that Wallerian degeneration produces signals for invasion of ED1+ macrophages to contralateral DRG.
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