In this study, we evaluated the expression of MCP-1 in the rat dorsal root ganglion (DRG) and spinal cord following axotomy and chronic constriction injury (CCI) of the sciatic nerve and L5 spinal nerve ligation (L5 SNL) using an immunohistochemical approach. MCP-1 expression in the DRG peaked and declined before the full onset of pain hypersensitivity following nerve injury. Spinal expression of MCP-1 peaked when mechanical allodynia was maximal, but then declined rapidly despite the remarkable persistence of mechanical allodynia. The results suggest that MCP-1 may participate in the initiation of neuropathic pain, rather than in its maintenance. Despite increased MCP-1 in small and large DRG neurons, a remarkable increase in MCP-1-IR terminals was observed in the spinal superficial laminae following CCI and L5SNL, but not following axotomy; however, in the deeper laminae, a considerable increase in MCP-1-IR terminals, which may originate from the large and injured L5 DRG neurons, was found after L5 SNL. Our results demonstrate that MCP-1 synthesized in DRG neurons may or may not be transported to the spinal cord depending on the type of peripheral nerve injury. Additionally, increased MCP-1 in both intact L4 and injured L5 DRG neurons may contribute to neuropathic pain hypersensitivity following L5 SNL.