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G-protein-coupled receptor 40 (GPR40)/free fatty acid receptor (FFAR) 1 is activated by long-chain fatty acids such as docosahexaenoic acid (DHA). Its receptor is expressed predominantly in the central nervous system (CNS) and in β-cells in the pancreatic Islets. We have already demonstrated that the intracerebroventricular administration of DHA or GW9508, a GPR40/FFAR1 agonist, suppresses formalin-induced pain behavior. It also attenuates complete Freund's adjuvant-induced mechanical allodynia and thermal hyperalgesia, suggesting that these effects occur by increasing β-endorphin release from propiomelanocortin neurons. Furthermore, we found that the brain GPR40/FFAR1 signaling may involve in the regulation of the descending pain control system, whereas the deletion of GPR40/FFAR1 might exacerbate mechanical allodynia in postoperative pain. Therefore, it is possible that the brain n-3 fatty acid-GPR40/FFAR1 signaling may play a key role in the modulation of the endogenous pain control system and emotional function. Here, we discuss the role of brain n-3 fatty acids-GPR40/FFAR1 signaling in a pain, and we review the current status and future prospects of the brain GPR40/FFAR1.

The role of brain n-3 fatty acids-GPR40/FFAR1 signaling in pain