Pain is a sensation induced by activation of the peripheral nociceptors when tissue is damaged by direct stimuli or has a possibility of damage. There exist nociceptors for detecting the noxious stimuli in periphery, and the nociceptive informations were transmitted via A delta- or C-fibers. Acute pain is caused by direct noxious stimuli, and chronic pains are produced by inflammation or nerve damage. The mechanisms of chronic pains are associated with the changes of cen-tral nervous system (CNS) as well as those in peripheral nocicpetors. Immune cells and neurotrophins are also involved in the mechanisms of chronic pain. Recently, there has been a tendency among pain researchers that chronic pain might be explained the plastic changes in the nociceptive synaptic transmission through the spinal cord. These are associated with changes in intracellular Ca(2+)concentration, subsequent intracellular signal transduction pathways, which result in changes in AMPA receptor dynamics. This sequential changes may induce allodynia and hyperalgesia observed in chronic pain patients. This review suggests new interpretation for pain mechanism and new approach for chronic pain.