• H Ueda and M Inoue.
• Department of Molecular Pharmacology and Neuroscience, Nagasaki University School of Pharmaceutical Sciences, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan. ueda@net.nagasaki-u.ac.jp
• Nippon Yakurigaku Zasshi. 2001 Aug 1;118(2):89-95.

AbstractNeuropathic pain associated with abnormal tactile and thermal responses that are extraterritorial to the injured nerve is known to be difficult to diagnose and treat because of clinical observation of limited responsiveness to opioids and non-steroidal anti-inflammatory drugs. To reproduce the different pathological changes observed in neuropathic pain patients, several laboratory animal models have been proposed. Recent studies using such models suggest the involvement of neuronal plasticity in pain pathways through nociceptive neurons. Our new experimental model using specific pain-producing molecules that clearly distinguish three different nociceptive fibers from each other reproduces neuropathic pain-like hyperalgesia and less sensitivity to morphine. After nerve injury, the nociceptive responses through type I neurons, which are polymodal C-fibers and drive NK1-receptor mechanisms in spinal pain transmission, were completely lost, but without changes in type II ones, which are polymodal C-fibers and drive NMDA receptor-mechanisms, while type III ones, which are capsaicin-insensitive (possibly A-fibers) and drive NMDA-receptor mechanisms, were markedly enhanced. Such pain transmission switch mechanisms are clearly consistent with clinical effectiveness including less sensitivity to morphine and more sensitivity to NMDA-antagonists. This article also presents currently used methods for experimental neuropathic pain models.

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