Peripheral nerve injury has been shown to result in ectopic spontaneous discharges on soma and injured sites of sensory neurons, thereby inducing neuropathic pain. With the increase of membrane proteins on soma and injured site neurons, the negatively charged sialic acids bind to the extal domains of membrane proteins, resulting in an increase of this charge. We therefore speculate that the electrophoretic velocity of injured neurons may be faster than non-injured neurons. The present study established rat models of neuropathic pain via chronic constriction injury. Results of the cell electrophoresis test revealed that the electrophoretic velocity of injured neuronal cells was faster than that of non-injured (control) cells. We then treated cells with di-valent cations of Ca2+and organic compounds with positive charges, polylysine to counteract the negatively charged sialic acids, or neuraminidase to speciifcally remove sialic acids from the membrane surface of injured neurons. All three treatments significantly reduced the electro-phoretic velocity of injured neuronal cells. These ifndings suggest that enhanced sialic acids on injured neurons may accelerate the electrophoretic velocity of injured neurons.