• Hirokazu Mizoguchi, Chizuko Watanabe, Akihiko Yonezawa, and Shinobu Sakurada.
• Department of Physiology and Anatomy, Tohoku Pharmaceutical University, Sendai 981-8558, Japan.
• Int Rev Neurobiol. 2009 Jan 1; 85: 249-60.

AbstractNeuropathic pain is one of the worst painful symptoms in clinic. It contains nerve-injured neuropathy, diabetic neuropathy, chronic inflammatory pain, cancer pain, and postherpes pain, and is characterized by a tactile allodynia and hyperalgesia. Neuropathic pain, especially the nerve-injured neuropathy, the diabetic neuropathy, and the cancer pain, is opioid resistant pain. Since the downregulation of mu-opioid receptors is observed in dorsal spinal cord, morphine and fentanyl could not provide marked antihyperalgesic/antiallodynic effects in the course neuropathic pain states. The downregulation of mu-opioid receptors is suggested to be mediated through the activation of NMDA receptors. Moreover, at the neuropathic pain states, the increased expression of voltage-dependent Na+ channels and Ca2+ channels are observed. Based on the above information concerned with the pathophysiology of neural changes in neuropathic pain states, new drug treatments for neuropathic pain, using ketamine, methadone, and gabapentin, have been developed. These drugs show remarkable effectiveness against hyperalgesia and allodynia during neuropathic pain states. Oxycodone is a mu-opioid receptor agonist, which has different pharmacological profiles with morphine. The remarkable effectiveness of oxycodone for neuropathic pain provides the possibility that mu-opioid receptor agonists, which have different pharmacological profile with morphine, can be used for the management of neuropathic pain.

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