摘要Recently, considerable progress in our understanding of the mechanisms of neuropathic pain has been made because of development of several suitable animal models. Neuronal sensitization is believed to play an important role in the pathogenesis of neuropathic pain following peripheral nerve injury.There is much evidence that nitric oxide (NO) is involved in the development and maintenance of pain following peripheral nerve injury. The main focus of this article will be on the recent development in understanding the importance of NO acting as a mediator or messenger in the nociceptive signal processing of neuropathic pain. This information suggests a specific avenue for development of more effective clinical medication for neuropathic pain following nerve injury.