A number of good animal models have been developed in recent years that provide insights into the mechanisms of neuropathic pain. It now becomes evident that there are two separate peripheral components influencing neuropathic pain: one dependent on the hyperexcitability of axotomized dorsal root ganglion (DRG) neurons and the other independent of this hyperexcitability. The purpose of this review is to consider one of these components, the hyperexcitability of axotomized DRG neurons, as one of the important mechanisms underlying neuropathic pain. Several hours after nerve lesions, some axotomized DRG neurons become hyperexcitable and begin to show ongoing discharges that last many days or weeks. These ectopic discharges then enter the spinal cord and induce central sensitization, the underlying central mechanism for the generation of pain and allodynia. Although the exact causes of the development of hyperexcitability and ectopic discharges are not clear, various ion channels seem to play important roles, particularly sodium channels. In addition, important modulatory factors for ectopic discharges are purinergic and adrenergic components of the sympathetic nervous system. These findings suggest that manipulating sodium channels and/or adrenergic and purinergic receptors on axotomized DRG cells may give neuropathic pain sufferers some relief that is not available from present treatment regimens.