Pathophysiological mechanisms of low back pain and radicular pain produced by lumbar disorders are still controversial. We have made experimental animal models and have elucidated the mechanisms of hyperalgesia, which is a pain related behavior, in these animals. We have not demonstrated that only mechanical compression of the nerve roots in the lumbar spine results in hyperalgesia in rat. We found that application of the nucleus pulposus to the nerve roots produces time-dependent reversible hyperalgesia in the affected hindpaw of the rat, and that the hyperalgesia is related to bioactive substances in the arachidonic acid cascade. We have also reported that inflammatory granulation tissue around the nerve root is related to hyperalgesia rather than the nucleus pulposus itself, and that mechanical compression to the nerve root after application of the nucleus pulposus produces different type of hyperalgesia. Collectively, not only mechanical compression of the cauda equina and nerve root but also various inflammatory substances are related to pathophysiological mechanisms of radicular pain in patients with lumbar disorders such as disc herniation. Elucidating pathophysiological mechanisms of pain-related behaviors such as hyperalgesia is important to establish a new strategy for the treatment of lumbar painful radiculopathy.