Abstract
Introduction: The goal of pain research is the establishment of new strategies for relieving pain in patients suffering from intolerable pain. Postoperative pain, that is, surgical incision-induced pain, is commonly encountered in a clinical setting, but little is known about its mechanisms. Methods and results: In this symposium, I will first present results showing that development of primary hyperalgesia and spread of secondary hyperalgesia following an experimental incision in human volunteers are caused by peripheral mechanisms, not by central mechanisms. I will then show that spinal mechanisms of postoperative pain in the adult rat are different from those of tissue injury-induced pain in conventionally used animal models. I will also show that spinal mechanisms of postoperative pain in neonatal rats are different from those in adult rats; one example is that postoperative pain is associated with activation of NMDA receptors of the spinal cord in neonatal rats but not in adult rats. Finally, I will show that different mouse strains have different sensitivities of postoperative pain, reflecting different characteristics of spinal dorsal horn neurons in the strains following surgical incision. Conclusions: The results suggest that pain intensity and pain mechanisms depend on the type of injury and on the age and genetic background of the individual. Since mechanisms of pain seen in a clinical setting may thus be different from those in animal models conventionally used, translational research should play more important roles in the field of pain research. [Jpn J Physiol 55 Suppl:S11 (2005)]
