4^th International Anesthesia and Pain Medicine Conference

Inflammation, tissue and nerve damage can cause persistent pain signed by increased response of noxious stimulus (hyperalgesia) and pain as a normal response of innoxious stimulus (allodynia). Postoperative pain is a form of pain cause by mechanical tissue damage. The synaptic plasticity of central sensitization is the basic mechanism of postoperative pain and the cause of persistent and establishment of hyperalgesia and allodynia. Central sensitization of the dorsal horn of the spinal cord is modulated by the production of glutamate neurotransmitter by the terminal primary afferent nerve root which activates the postsynapse receptor and or by the effect of the quantity and type of postsynaptic membrane receptor. The AMPA glutamate ionotropic receptor and its interaction with the NMDA receptor is postulated to be involved in the neurophysiology of postoperative incisional pain which may develop to persistent and chronic pain. The regulation interaction of the AMPA and NMDA receptors plays a role in Long Term Potentiation (LTP). Some studies conclude peripheral inflammation cause changes in the subunit AMPA

trafficking through the NMDA receptor that triggers the protein kinase activation at the dorsal horn and this change contributes in the central sensitization in increasing and prolong the persistent inflammation pain. Some

factors are involved in the nociception process in the spinal cord related to the trafficking of AMPA receptor such as subunit composition, phosphorylation regulation and protein interaction.