The NMDA receptor, pain and central sensitization

摘要: Pain hypersensitivity mechanistically results from two potential sources, peripheral sensitization [1, 2] and central [3]. Peripheral is an increase in the transduction sensitivity of primary afferent nociceptors. It has been shown that a variety molecules physiochemical conditions can sensitize nociceptors [4], either by changing receptors, such as heat sensitive vanilloid receptor VR1 [5] or phosphorylation sodium channels terminal increasing excitability [6]. Central contrast neurons within nervous system (CNS), particularly involving dorsal horn spinal cord. This modifies responsiveness to subsequent low high threshold sensory inputs [7], producing pain both at site tissue damage (primary hyperalgesia) surrounding non-damaged (secondary [8].