Peripheral nerve injury can result in formation of a neuroma, which is often associated with heightened sensitivity to normally innocuous stimuli as well as spontaneous dysesthesia and pain. The onset and persistence of neuropathic pain have been linked to spontaneous ectopic electrogenesis in axons within neuromas, suggesting an involvement of voltage-gated sodium channels. Sodium channel isoforms Na_V1.3, Na_V1.7 and Na_V1.8 have been shown to accumulate in chronic painful human neuromas, while, to date, only Na_V1.3 has been reported to accumulate within experimental neuromas. Although recent evidence strongly support a major contribution for Na_V1.7 in nociception, the expression of Na_V1.7 in injured axons within acute neuromas has not been studied. The current study examined whether Na_V1.7 accumulates in experimental rat neuromas. We further investigated whether activated (phosphorylated) mitogen-activated protein (MAP) kinase ERK1/2, which is known to modulate Na_V1.7 properties, is co-localized with Na_V1.7 within axons in neuromas. We demonstrate increased levels of Na_V1.7 in experimental rat sciatic nerve neuromas, 2 weeks after nerve ligation and transaction. We further show elevated levels of phosphorylated ERK1/2 within individual neuroma axons that exhibit Na_V1.7 accumulation. These results extend previous descriptions of sodium channel and MAP kinase accumulation within experimental and human neuromas, and suggest that targeted blockade of Na_V1.7 or ERK1/2 may provide a strategy for amelioration of chronic pain that often follows nerve injury and formation of neuromas.